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Possible new mechanisms of primary drug resistance in NSCLC with EGFR mutation treated with Osimertinib
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-02-05 DOI: 10.1002/iub.70002
Lujing Shao, Tong Li, Xinyan Jia, Xinyu Zhang, Qi Li, Chunyan Dong

In this study, a patient with lung adenocarcinoma harboring an EGFR mutation exhibited primary resistance to the targeted EGFR inhibitor Osimertinib after 2 months of treatment. As the disease advanced, further genetic analysis revealed the emergence of additional mutations in ARID1A, NTRK1, and ZRSR2, alongside the existing EGFR mutation. Subsequent treatment with Pemetrexed resulted in a significant reduction in liver metastases. Protein mass spectrometry sequencing and immunohistochemical analysis collectively indicated that the PI3K/mTOR pathway mediates the mechanism through which these gene mutations confer primary drug resistance. Evidence demonstrates that the co-occurrence of EGFR and ARID1A mutations diminishes the efficacy of EGFR tyrosine kinase inhibitors (EGFR TKIs). Consequently, it is hypothesized that mutations in NTRK1 and ZRSR2, which are implicated in the PI3K/mTOR pathway, contribute to the primary resistance observed with Osimertinib treatment. In this case, the illness was effectively managed through prompt adjustments to the treatment regimen and the rapid administration of chemotherapy drugs. This finding also constitutes the first evidence that mutations in NTRK1 and ZRSR2 are pivotal in the development of primary resistance to Osimertinib. Consequently, it is imperative to conduct genetic testing at the earliest opportunity and modify the treatment plan accordingly.

{"title":"Possible new mechanisms of primary drug resistance in NSCLC with EGFR mutation treated with Osimertinib","authors":"Lujing Shao,&nbsp;Tong Li,&nbsp;Xinyan Jia,&nbsp;Xinyu Zhang,&nbsp;Qi Li,&nbsp;Chunyan Dong","doi":"10.1002/iub.70002","DOIUrl":"10.1002/iub.70002","url":null,"abstract":"<p>In this study, a patient with lung adenocarcinoma harboring an EGFR mutation exhibited primary resistance to the targeted EGFR inhibitor Osimertinib after 2 months of treatment. As the disease advanced, further genetic analysis revealed the emergence of additional mutations in ARID1A, NTRK1, and ZRSR2, alongside the existing EGFR mutation. Subsequent treatment with Pemetrexed resulted in a significant reduction in liver metastases. Protein mass spectrometry sequencing and immunohistochemical analysis collectively indicated that the PI3K/mTOR pathway mediates the mechanism through which these gene mutations confer primary drug resistance. Evidence demonstrates that the co-occurrence of EGFR and ARID1A mutations diminishes the efficacy of EGFR tyrosine kinase inhibitors (EGFR TKIs). Consequently, it is hypothesized that mutations in NTRK1 and ZRSR2, which are implicated in the PI3K/mTOR pathway, contribute to the primary resistance observed with Osimertinib treatment. In this case, the illness was effectively managed through prompt adjustments to the treatment regimen and the rapid administration of chemotherapy drugs. This finding also constitutes the first evidence that mutations in NTRK1 and ZRSR2 are pivotal in the development of primary resistance to Osimertinib. Consequently, it is imperative to conduct genetic testing at the earliest opportunity and modify the treatment plan accordingly.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iub.70002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Zinc finger protein 169 promotes tumor progress of hepatocellular cancer via up-regulating cyclin-dependent kinase 19
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-27 DOI: 10.1002/iub.2943
Chaoquan Hu, Aizier Ainiwaer, Ying Lu, Jiaxing Li, Yongmei Fu, Jun Luo, Baijun Wu, Peng Yin, Xiao Hu, Yao Sun, Hong Li, He Lu, Zheng Dong

Hepatocellular carcinoma (HCC) ranks among the most prevalent types of cancer globally. Zinc finger protein 169 (ZNF169) holds significant importance as a transcription factor, yet its precise function in HCC remains to be elucidated. This study aims to examine the clinical importance, biological functions, and molecular pathways associated with ZNF169 in the development of HCC. The study employed lentiviral transduction for ZNF169 overexpression and the use of small interfering RNAs (siRNAs) to suppress its expression. ZNF169 was upregulated in HCC tissues and cell lines. Additionally, HCC patients exhibiting elevated ZNF169 levels experienced reduced overall survival, shorter disease-free survival, and diminished progression-free survival. Silencing of ZNF169 inhibited cell proliferation, migration, and cell cycle progression. Whereas ectopic expression of ZNF169 promoted HCC progression in vivo and ex vivo. Subsequently, Pearson analysis results showed that cyclin-dependent kinase 19 (CDK19) was positively correlated with ZNF169 levels in HCC using TCGA dataset. Luciferase assay findings indicated a potential interaction between ZNF169 and CDK19 promoter. Additionally, our data showed that CDK19 expression levels were elevated in HCC tissues, and patients with higher CDK19 expression faced a poorer prognosis. Furthermore, recovery experiments demonstrated that CDK19 could reverse the impact of ZNF169 on HCC cell amplification. Our findings indicate that ZNF169 promotes HCC progression by upregulating CDK19, highlighting its role as a therapeutic target or prognostic biomarker for HCC.

{"title":"Zinc finger protein 169 promotes tumor progress of hepatocellular cancer via up-regulating cyclin-dependent kinase 19","authors":"Chaoquan Hu,&nbsp;Aizier Ainiwaer,&nbsp;Ying Lu,&nbsp;Jiaxing Li,&nbsp;Yongmei Fu,&nbsp;Jun Luo,&nbsp;Baijun Wu,&nbsp;Peng Yin,&nbsp;Xiao Hu,&nbsp;Yao Sun,&nbsp;Hong Li,&nbsp;He Lu,&nbsp;Zheng Dong","doi":"10.1002/iub.2943","DOIUrl":"10.1002/iub.2943","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) ranks among the most prevalent types of cancer globally. Zinc finger protein 169 (ZNF169) holds significant importance as a transcription factor, yet its precise function in HCC remains to be elucidated. This study aims to examine the clinical importance, biological functions, and molecular pathways associated with ZNF169 in the development of HCC. The study employed lentiviral transduction for ZNF169 overexpression and the use of small interfering RNAs (siRNAs) to suppress its expression. ZNF169 was upregulated in HCC tissues and cell lines. Additionally, HCC patients exhibiting elevated ZNF169 levels experienced reduced overall survival, shorter disease-free survival, and diminished progression-free survival. Silencing of ZNF169 inhibited cell proliferation, migration, and cell cycle progression. Whereas ectopic expression of ZNF169 promoted HCC progression in vivo and ex vivo. Subsequently, Pearson analysis results showed that cyclin-dependent kinase 19 (CDK19) was positively correlated with ZNF169 levels in HCC using TCGA dataset. Luciferase assay findings indicated a potential interaction between ZNF169 and CDK19 promoter. Additionally, our data showed that CDK19 expression levels were elevated in HCC tissues, and patients with higher CDK19 expression faced a poorer prognosis. Furthermore, recovery experiments demonstrated that CDK19 could reverse the impact of ZNF169 on HCC cell amplification. Our findings indicate that ZNF169 promotes HCC progression by upregulating CDK19, highlighting its role as a therapeutic target or prognostic biomarker for HCC.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Deciphering the senescence-based tumoral heterogeneity and characteristics in pancreatic cancer: Results from parallel bulk and single-cell transcriptome data
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-26 DOI: 10.1002/iub.70001
Yeting Lu, Shuo Han, Jing Hu, Kaiji Lv, Yi Ruan, Gong Cheng, Jing Zhang, Xiang Wu, Zeming Weng, Xinhua Zhou

The prevalent intra- and intertumoral heterogeneity results in undesirable prognosis and therapy failure of pancreatic cancer, potentially resulting from cellular senescence. Herein, integrated analysis of bulk and single-cell RNA-seq profiling was conducted to characterize senescence-based heterogeneity in pancreatic cancer. Publicly available bulk and single-cell RNA sequencing from pancreatic cancer patients were gathered from TCGA-PAAD, PACA-AU, PACA-CA, and GSE154778 datasets. The activity of three senescence-related pathways (cell cycle, DNA repair, and inflammation) was scored utilizing ssGSEA algorithm. A series of functional verifications of crucial genes were accomplished in patient tissue and pancreatic cancer cells. Based upon them, unsupervised clustering analysis was executed to classify pancreatic cancer samples into distinct senescence-based clusters at the bulk and single-cell levels. For single-cell transcriptome profiling, cell clustering and annotation were implemented, and malignant cells were recognized utilizing infercnv algorithm. Two senescence-based clusters were established and highly reproducible at the bulk level, with the heterogeneity in prognosis, clinicopathological features, genomic CNVs, oncogenic pathway activity, immune microenvironment and immune checkpoints. Senescence-relevant gene CHGA, UBE2C and MCM10 were proved to correlate with the migration and prognosis of pancreatic cancer. At the single-cell level, seven cell types were annotated, comprising ductal cells 1, ductal cells 2, fibroblasts, macrophages, T cells, stellate cells, and endothelial cells. The senescence-based classification was also proven at the single-cell level. Ductal cells were classified as malignant cells and non-malignant cells. In the tumor microenvironment of malignant cells, hypoxia and angiogenesis affected senescent phenotype. The heterogeneity in senescence was also observed between and within cell types. Altogether, our findings unveil that cellular senescence contributes to intra- and intertumoral heterogeneity in pancreatic cancer, which might facilitate the development of therapeutics and precision therapy in pancreatic cancer.

{"title":"Deciphering the senescence-based tumoral heterogeneity and characteristics in pancreatic cancer: Results from parallel bulk and single-cell transcriptome data","authors":"Yeting Lu,&nbsp;Shuo Han,&nbsp;Jing Hu,&nbsp;Kaiji Lv,&nbsp;Yi Ruan,&nbsp;Gong Cheng,&nbsp;Jing Zhang,&nbsp;Xiang Wu,&nbsp;Zeming Weng,&nbsp;Xinhua Zhou","doi":"10.1002/iub.70001","DOIUrl":"10.1002/iub.70001","url":null,"abstract":"<p>The prevalent intra- and intertumoral heterogeneity results in undesirable prognosis and therapy failure of pancreatic cancer, potentially resulting from cellular senescence. Herein, integrated analysis of bulk and single-cell RNA-seq profiling was conducted to characterize senescence-based heterogeneity in pancreatic cancer. Publicly available bulk and single-cell RNA sequencing from pancreatic cancer patients were gathered from TCGA-PAAD, PACA-AU, PACA-CA, and GSE154778 datasets. The activity of three senescence-related pathways (cell cycle, DNA repair, and inflammation) was scored utilizing ssGSEA algorithm. A series of functional verifications of crucial genes were accomplished in patient tissue and pancreatic cancer cells. Based upon them, unsupervised clustering analysis was executed to classify pancreatic cancer samples into distinct senescence-based clusters at the bulk and single-cell levels. For single-cell transcriptome profiling, cell clustering and annotation were implemented, and malignant cells were recognized utilizing infercnv algorithm. Two senescence-based clusters were established and highly reproducible at the bulk level, with the heterogeneity in prognosis, clinicopathological features, genomic CNVs, oncogenic pathway activity, immune microenvironment and immune checkpoints. Senescence-relevant gene CHGA, UBE2C and MCM10 were proved to correlate with the migration and prognosis of pancreatic cancer. At the single-cell level, seven cell types were annotated, comprising ductal cells 1, ductal cells 2, fibroblasts, macrophages, T cells, stellate cells, and endothelial cells. The senescence-based classification was also proven at the single-cell level. Ductal cells were classified as malignant cells and non-malignant cells. In the tumor microenvironment of malignant cells, hypoxia and angiogenesis affected senescent phenotype. The heterogeneity in senescence was also observed between and within cell types. Altogether, our findings unveil that cellular senescence contributes to intra- and intertumoral heterogeneity in pancreatic cancer, which might facilitate the development of therapeutics and precision therapy in pancreatic cancer.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CDKN3 as a key regulator of G2M phase in triple-negative breast cancer: Insights from multi-transcriptomic analysis
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-26 DOI: 10.1002/iub.2922
Haodi Ma, Yirui Dong, Jiayu Zheng, Shunshun Zhang, Siya Tang, Junxiang Wang, Zhifeng Qu, Xiucheng Li, Li Zeng, Kena Song, Chunyan Liu, Linlin Shi, Qinan Yin, Xuewei Zheng

Triple-negative breast cancer (TNBC) remains a significant global health challenge, emphasizing the need for precise identification of patients with specific therapeutic targets and those at high risk of metastasis. This study aimed to identify novel therapeutic targets for personalized treatment of TNBC patients by elucidating their roles in cell cycle regulation. Using weighted gene co-expression network analysis (WGCNA), we identified 83 hub genes by integrating gene expression profiles with clinical pathological grades. A machine learning-based integrative approach further pinpointed 12 prognostic genes, among which CDKN3 exhibited the highest hazard ratio and the most adverse impact on overall survival (OS) in BC patients. Additionally, CDKN3 was identified as an independent prognostic factor for OS prediction. CDKN3 overexpression was confirmed in BC patients and validated at both mRNA and protein levels in BC cells. Knockdown of CDKN3 significantly inhibited the migration and proliferation of BC cells. Cell cycle pathway analysis revealed significant enrichment in G2M-associated pathways in BC patients, with multi-transcriptomic data indicating a close association between enhanced G2M cell cycle activity and CDKN3 upregulation in basal cancer subtypes. Pseudotime analysis further suggested CDKN3 upregulation during the G2M phase at the terminal trajectory of basal cancer subtypes, implying that CDKN3 may drive BC cell progression by promoting G2M cell cycle activity. Mechanistically, CDKN3 knockdown induced G2M cell cycle arrest in TNBC cells by downregulating CCNB2. In conclusion, CDKN3 knockdown effectively inhibits TNBC by arresting the G2M cell cycle, underscoring CDKN3 as a promising therapeutic target in TNBC treatment.

{"title":"CDKN3 as a key regulator of G2M phase in triple-negative breast cancer: Insights from multi-transcriptomic analysis","authors":"Haodi Ma,&nbsp;Yirui Dong,&nbsp;Jiayu Zheng,&nbsp;Shunshun Zhang,&nbsp;Siya Tang,&nbsp;Junxiang Wang,&nbsp;Zhifeng Qu,&nbsp;Xiucheng Li,&nbsp;Li Zeng,&nbsp;Kena Song,&nbsp;Chunyan Liu,&nbsp;Linlin Shi,&nbsp;Qinan Yin,&nbsp;Xuewei Zheng","doi":"10.1002/iub.2922","DOIUrl":"10.1002/iub.2922","url":null,"abstract":"<p>Triple-negative breast cancer (TNBC) remains a significant global health challenge, emphasizing the need for precise identification of patients with specific therapeutic targets and those at high risk of metastasis. This study aimed to identify novel therapeutic targets for personalized treatment of TNBC patients by elucidating their roles in cell cycle regulation. Using weighted gene co-expression network analysis (WGCNA), we identified 83 hub genes by integrating gene expression profiles with clinical pathological grades. A machine learning-based integrative approach further pinpointed 12 prognostic genes, among which CDKN3 exhibited the highest hazard ratio and the most adverse impact on overall survival (OS) in BC patients. Additionally, CDKN3 was identified as an independent prognostic factor for OS prediction. CDKN3 overexpression was confirmed in BC patients and validated at both mRNA and protein levels in BC cells. Knockdown of CDKN3 significantly inhibited the migration and proliferation of BC cells. Cell cycle pathway analysis revealed significant enrichment in G2M-associated pathways in BC patients, with multi-transcriptomic data indicating a close association between enhanced G2M cell cycle activity and CDKN3 upregulation in basal cancer subtypes. Pseudotime analysis further suggested CDKN3 upregulation during the G2M phase at the terminal trajectory of basal cancer subtypes, implying that CDKN3 may drive BC cell progression by promoting G2M cell cycle activity. Mechanistically, CDKN3 knockdown induced G2M cell cycle arrest in TNBC cells by downregulating CCNB2. In conclusion, CDKN3 knockdown effectively inhibits TNBC by arresting the G2M cell cycle, underscoring CDKN3 as a promising therapeutic target in TNBC treatment.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The up-regulation of RIPK3 mediated by ac4C modification promotes oxidative stress-induced granulosa cell senescence by inhibiting the Nrf2/HO-1 pathway
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-25 DOI: 10.1002/iub.2944
Wanjun Zhang, Jiahao Zhang, Yile Zhang, Jun Zhai, Bo Sun, Yihong Guo, Fang Wang

Abnormality of granulosa cells (GCs) is the critical cause of follicular atresia in premature ovarian failure (POF). RIPK3 is highly expressed in GCs derived from atretic follicles. We focus on uncovering how RIPK3 contributes to ovarian GC senescence. Primary GCs were treated with H₂O₂ to induce senescence. ROS was detected via DCFH-DA staining. Levels of senescence-related molecules and SA-β-Gal activity were examined. Cyclophosphamide was administered to mice to induce POF. The impact of RIPK3 on atretic follicles and sex hormones was evaluated through HE staining and ELISA, respectively. The acRIP-qPCR analysis of RIPK3 ac4C levels, RIP detection for interaction between RIPK3 and NAT10, and actinomycin D treatment to detect RIPK3 degradation were conducted. In H2O2-treated GCs and POF mouse ovaries, levels of RIPK3, ROS, senescence-related molecules, as well as SA-β-Gal activity, were all up-regulated, and this effect was suppressed by RIPK3 inhibition. RIPK3 interference reduced atretic follicles and FSH levels while increasing AMH and E2 levels. Nrf2 and HO-1 content were diminished in the models, whereas si-RIPK3 facilitated their expression. The effect of si-RIPK3 on decreased levels of ROS and senescence-related molecules was reversed by ML385. H2O2 decreased RIPK3 mRNA degradation and increased its ac4C modification. The ac4C modifying enzyme NAT10 was up-regulated in the models, and NAT10 enhanced RIPK3 mRNA stability through ac4C modification. NAT10 knockdown mitigated ovarian GC senescence by inhibiting RIPK3 expression. The promotion of RIPK3 mRNA stability through ac4C modification by NAT10, in turn, affects the Nrf2/HO-1 pathway and promotes ovarian GC senescence.

{"title":"The up-regulation of RIPK3 mediated by ac4C modification promotes oxidative stress-induced granulosa cell senescence by inhibiting the Nrf2/HO-1 pathway","authors":"Wanjun Zhang,&nbsp;Jiahao Zhang,&nbsp;Yile Zhang,&nbsp;Jun Zhai,&nbsp;Bo Sun,&nbsp;Yihong Guo,&nbsp;Fang Wang","doi":"10.1002/iub.2944","DOIUrl":"10.1002/iub.2944","url":null,"abstract":"<p>Abnormality of granulosa cells (GCs) is the critical cause of follicular atresia in premature ovarian failure (POF). RIPK3 is highly expressed in GCs derived from atretic follicles. We focus on uncovering how RIPK3 contributes to ovarian GC senescence. Primary GCs were treated with H₂O₂ to induce senescence. ROS was detected via DCFH-DA staining. Levels of senescence-related molecules and SA-β-Gal activity were examined. Cyclophosphamide was administered to mice to induce POF. The impact of RIPK3 on atretic follicles and sex hormones was evaluated through HE staining and ELISA, respectively. The acRIP-qPCR analysis of RIPK3 ac4C levels, RIP detection for interaction between RIPK3 and NAT10, and actinomycin D treatment to detect RIPK3 degradation were conducted. In H<sub>2</sub>O<sub>2</sub>-treated GCs and POF mouse ovaries, levels of RIPK3, ROS, senescence-related molecules, as well as SA-β-Gal activity, were all up-regulated, and this effect was suppressed by RIPK3 inhibition. RIPK3 interference reduced atretic follicles and FSH levels while increasing AMH and E2 levels. Nrf2 and HO-1 content were diminished in the models, whereas si-RIPK3 facilitated their expression. The effect of si-RIPK3 on decreased levels of ROS and senescence-related molecules was reversed by ML385. H<sub>2</sub>O<sub>2</sub> decreased RIPK3 mRNA degradation and increased its ac4C modification. The ac4C modifying enzyme NAT10 was up-regulated in the models, and NAT10 enhanced RIPK3 mRNA stability through ac4C modification. NAT10 knockdown mitigated ovarian GC senescence by inhibiting RIPK3 expression. The promotion of RIPK3 mRNA stability through ac4C modification by NAT10, in turn, affects the Nrf2/HO-1 pathway and promotes ovarian GC senescence.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CRYAB is upregulated and predicts clinical prognosis in kidney renal clear cell carcinoma
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-24 DOI: 10.1002/iub.2938
Hao Ren, Xinyu Chen, Meiling Ji, Wengang Song, Lili Cao, Xiaohong Guo

Clear cell renal cell carcinoma (KIRC) is the most prevalent subtype of renal cell carcinoma (RCC), accounting for 70% to 80% of all RCC cases. The CRYAB (αB-crystallin) gene is broadly expressed across various human tissues, yet its role in KIRC progression remains unclear. This study aims to elucidate the function of CRYAB in KIRC progression and to assess its potential as a biomarker for early diagnosis, therapeutic targeting, and prognosis. In our report, we found that CRYAB was dramatically upregulated in KIRC, and its expression was associated with TNM stage, pathological stage, and age. Also, patients with higher CRYAB expression exhibited poor survival and prognosis. CRYAB overexpression led to enhanced tumor cell proliferation. Vice versa, CRYAB downregulation resulted in decreased cell proliferation in vitro. Mechanistically, Gene set enrichment analysis plots showed the enrichment of cell survival. Consistently, these effects were associated with increased AKT signaling and BCL-2 expression. Furthermore, we also observed that CRYAB expression levels were negatively correlated with immunocyte infiltration. In conclusion, these findings suggested that CRYAB could be regarded as a latent biomarker for early diagnosis, therapeutic targeting, and prognosis.

{"title":"CRYAB is upregulated and predicts clinical prognosis in kidney renal clear cell carcinoma","authors":"Hao Ren,&nbsp;Xinyu Chen,&nbsp;Meiling Ji,&nbsp;Wengang Song,&nbsp;Lili Cao,&nbsp;Xiaohong Guo","doi":"10.1002/iub.2938","DOIUrl":"10.1002/iub.2938","url":null,"abstract":"<p>Clear cell renal cell carcinoma (KIRC) is the most prevalent subtype of renal cell carcinoma (RCC), accounting for 70% to 80% of all RCC cases. The CRYAB (αB-crystallin) gene is broadly expressed across various human tissues, yet its role in KIRC progression remains unclear. This study aims to elucidate the function of CRYAB in KIRC progression and to assess its potential as a biomarker for early diagnosis, therapeutic targeting, and prognosis. In our report, we found that CRYAB was dramatically upregulated in KIRC, and its expression was associated with TNM stage, pathological stage, and age. Also, patients with higher CRYAB expression exhibited poor survival and prognosis. CRYAB overexpression led to enhanced tumor cell proliferation. Vice versa, CRYAB downregulation resulted in decreased cell proliferation in vitro. Mechanistically, Gene set enrichment analysis plots showed the enrichment of cell survival. Consistently, these effects were associated with increased AKT signaling and BCL-2 expression. Furthermore, we also observed that CRYAB expression levels were negatively correlated with immunocyte infiltration. In conclusion, these findings suggested that CRYAB could be regarded as a latent biomarker for early diagnosis, therapeutic targeting, and prognosis.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
APOC1 inhibit NKTCL doxorubicin sensitivity by promoting mitophagy APOC1通过促进线粒体自噬抑制NKTCL对阿霉素的敏感性。
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-16 DOI: 10.1002/iub.2942
Sa Xiao, Jing Kuang, Jiamei yang, Haili Wang, Yuanyuan sun, Haipeng Zhang, Zhongyu Zhang, Mengyuan Shi, Kai Qi, Miao Jiang, Yanyan Zhang, Qingjiang Chen, Xudong Zhang

NKTCL is a highly aggressive malignant tumor, especially prevalent in the southern regions of China. Although chemotherapy regimens based on ADM have achieved certain therapeutic effects in early treatment, the issue of ADM resistance severely limits the therapeutic efficacy and makes it difficult to improve patient survival rates. Our research results indicate that the expression level of APOC1 is closely related to the sensitivity of NKTCL cells to ADM. The upregulation of APOC1 may promote mitophagy, clear damaged mitochondria, stabilize the intracellular environment, and enhance the tolerance of tumor cells to ADM. Furthermore, APOC1 may further affect the formation of mitophagy and drug resistance by activating specific signaling pathways, such as the STAT3 signaling pathway. Animal experiments further confirm the conclusions of in vitro experiments, showing that APOC1 regulates mitophagy through p-STAT3Tyr705, thereby promoting the drug resistance of NKTCL. These findings provide a new perspective for the development of novel therapeutic strategies targeting APOC1 and its associated signaling pathways, which may help overcome the issue of ADM resistance in NKTCL.

NKTCL是一种高度侵袭性的恶性肿瘤,尤其常见于中国南方地区。虽然基于ADM的化疗方案在早期治疗中取得了一定的治疗效果,但ADM耐药问题严重限制了治疗效果,使患者生存率难以提高。我们的研究结果表明,APOC1的表达水平与NKTCL细胞对adm的敏感性密切相关,其表达上调可促进线粒体自噬,清除受损线粒体,稳定细胞内环境,增强肿瘤细胞对adm的耐受性,并可能通过激活特定的信号通路,如STAT3信号通路,进一步影响线粒体自噬的形成和耐药性。动物实验进一步证实了体外实验的结论,APOC1通过p-STAT3Tyr705调控线粒体自噬,从而促进NKTCL的耐药。这些发现为开发针对APOC1及其相关信号通路的新型治疗策略提供了新的视角,这可能有助于克服NKTCL的ADM抗性问题。
{"title":"APOC1 inhibit NKTCL doxorubicin sensitivity by promoting mitophagy","authors":"Sa Xiao,&nbsp;Jing Kuang,&nbsp;Jiamei yang,&nbsp;Haili Wang,&nbsp;Yuanyuan sun,&nbsp;Haipeng Zhang,&nbsp;Zhongyu Zhang,&nbsp;Mengyuan Shi,&nbsp;Kai Qi,&nbsp;Miao Jiang,&nbsp;Yanyan Zhang,&nbsp;Qingjiang Chen,&nbsp;Xudong Zhang","doi":"10.1002/iub.2942","DOIUrl":"10.1002/iub.2942","url":null,"abstract":"<p>NKTCL is a highly aggressive malignant tumor, especially prevalent in the southern regions of China. Although chemotherapy regimens based on ADM have achieved certain therapeutic effects in early treatment, the issue of ADM resistance severely limits the therapeutic efficacy and makes it difficult to improve patient survival rates. Our research results indicate that the expression level of APOC1 is closely related to the sensitivity of NKTCL cells to ADM. The upregulation of APOC1 may promote mitophagy, clear damaged mitochondria, stabilize the intracellular environment, and enhance the tolerance of tumor cells to ADM. Furthermore, APOC1 may further affect the formation of mitophagy and drug resistance by activating specific signaling pathways, such as the STAT3 signaling pathway. Animal experiments further confirm the conclusions of in vitro experiments, showing that APOC1 regulates mitophagy through p-STAT3<sup>Tyr705</sup>, thereby promoting the drug resistance of NKTCL. These findings provide a new perspective for the development of novel therapeutic strategies targeting APOC1 and its associated signaling pathways, which may help overcome the issue of ADM resistance in NKTCL.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Tinagl1 restores tamoxifen sensitivity and blocks fibronectin-induced EMT by simultaneously blocking the EGFR and β1-integrin/FAK signaling pathways in tamoxifen-resistant breast cancer cells Tinagl1通过同时阻断他莫昔芬耐药乳腺癌细胞中的EGFR和β1-整合素/FAK信号通路,恢复他莫昔芬敏感性并阻断纤维连接素诱导的EMT。
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-16 DOI: 10.1002/iub.2940
Jie Yuan, Li Yuan, Li Yang, Arunachalam Chinnathambi, Sulaiman Ali Alharbi, Jun Huang, Bei Wang, Shuqi Zhang, Changsheng Wei, Chengyu Luo

Tamoxifen (TAM) is employed to treat premenopausal ER-positive breast cancer patients, but TAM resistance is the main reason affecting its efficacy. Thus, addressing TAM resistance is crucial for improving therapeutic outcomes. This study explored the potential role of Tinagl1, a secreted extracellular matrix protein, whose expression is compromised in TAM-resistant MCF-7 breast cancer cells (MCF-7R). We discovered that Tinagl1 plays a pivotal role in countering TAM resistance by inhibiting the EGFR and β1-integrin/focal adhesion kinase (FAK) signaling pathways, both of which are abnormally activated in MCF-7R cells and contribute to the resistance mechanism. Our data showed that the expression level of Tinagl1 in MCF-7R cells was lower compared to their wild-type counterparts, and TAM could further reduce Tinagl1 expression in MCF-7R cells, which was consistent with our microarray results. Moreover, Tinagl1 could restore the sensitivity of MCF-7R cells to TAM and inhibit the motility of MCF-7R cells by regulating epithelial-mesenchymal transition (EMT) in vitro and in vivo experiments. In addition, the level of Tinagl1 in TAM-resistant breast cancer samples was significantly lower than that in their matched primary tumors. Analysis of an online database further indicated that high Tinagl1 expression correlates with better recurrence-free survival (RFS), particularly in patients with ER-positive, HER2-negative breast cancer. Overall, this study positions Tinagl1 not only as a potential prognostic marker but also as a promising therapeutic target.

三苯氧胺(Tamoxifen, TAM)用于治疗绝经前er阳性乳腺癌患者,TAM耐药是影响其疗效的主要原因。因此,解决TAM耐药性对改善治疗效果至关重要。这项研究探索了分泌的细胞外基质蛋白Tinagl1的潜在作用,其表达在tam耐药的MCF-7乳腺癌细胞(MCF-7R)中受损。我们发现,Tinagl1通过抑制EGFR和β1-整合素/局灶粘附激酶(FAK)信号通路,在对抗TAM耐药中发挥关键作用,这两种信号通路在MCF-7R细胞中都异常激活,并参与耐药机制。我们的数据显示,与野生型细胞相比,MCF-7R细胞中Tinagl1的表达水平较低,TAM可以进一步降低MCF-7R细胞中Tinagl1的表达,这与我们的芯片结果一致。此外,在体外和体内实验中,Tinagl1可以通过调节上皮-间质转化(epithelial-mesenchymal transition, EMT),恢复MCF-7R细胞对TAM的敏感性,抑制MCF-7R细胞的运动。此外,tam耐药乳腺癌样本中的Tinagl1水平明显低于与其匹配的原发肿瘤。在线数据库的分析进一步表明,高Tinagl1表达与更好的无复发生存(RFS)相关,特别是在er阳性,her2阴性乳腺癌患者中。总的来说,这项研究不仅将Tinagl1定位为潜在的预后标志物,而且作为一个有希望的治疗靶点。
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引用次数: 0
Overexpression of RGPR-p117 reveals anticancer effects by regulating multiple signaling pathways in bone metastatic human breast cancer MDA-MB-231 cells RGPR-p117的过表达通过调节骨转移性人乳腺癌MDA-MB-231细胞的多种信号通路揭示了其抗癌作用。
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-08 DOI: 10.1002/iub.2939
Masayoshi Yamaguchi, Tomiyasu Murata, Noriaki Shimokawa

The role of RGPR-p117, a transcription factor, which binds to the TTGGC motif in the promoter region of the regucalcin gene, in cell regulation remains to be investigated. This study elucidated whether RGPR-p117 regulates the activity of triple-negative human breast cancer MDA-MB-231 cells in vitro. The wild-type and RGPR-p117-overexpressing cancer cells were cultured in DMEM supplemented with fetal bovine serum. RGPR-p117 overexpression suppressed colony formation and growth of cancer cells. Stimulatory effects of epidermal growth factor on cell growth were blocked by RGPR-p117 overexpression. Wild-type cell proliferation was repressed by cell cycle and intracellular signaling inhibitors. These effects were not potentiated in transfectants. Overexpressed RGPR-p117 protected cancer cells against apoptosis inducers. Mechanistic results showed that RGPR-p117 overexpression decreased the expression of Ras, PI3-kinase, Akt, mitogen-activated protein kinase, and mTOR, which are involved in cell growth, while it elevated the levels of the cancer cell suppressor p53, Rb, p21, and regucalcin. Overexpression of RGPR-p117 suppressed cancer cell migration and adhesion. Interestingly, osteoblastic MC3T3-E1 cells or macrophage RAW264.7 cells involved in the bone microenvironment were impaired by coculture with MDA-MB-231 cells. The effects of cancer cells were blocked by transfection. Coculture with conditioned medium obtained from breast cancer cells repressed proliferation and enhanced the death of osteoblastic cells and macrophages. A TNF-α signaling inhibitor blocked these effects. Thus, overexpressed RGPR-p117 was found to suppress the activity of breast cancer cells by regulating various signaling processes, providing new insight into cellular signaling regulation.

RGPR-p117是一种转录因子,它与regucalcin基因启动子区域的TTGGC基序结合,在细胞调控中的作用仍有待研究。本研究阐明了RGPR-p117是否在体外调控三阴性人乳腺癌MDA-MB-231细胞的活性。在添加胎牛血清的DMEM中培养野生型和过表达rgpr -p117的癌细胞。RGPR-p117过表达抑制肿瘤细胞集落形成和生长。表皮生长因子对细胞生长的刺激作用被RGPR-p117过表达阻断。细胞周期和细胞内信号抑制剂可抑制野生型细胞的增殖。这些效应在转染物中没有增强。过表达的RGPR-p117保护癌细胞免受凋亡诱导剂的影响。机制结果表明,RGPR-p117过表达降低了参与细胞生长的Ras、pi3激酶、Akt、丝裂原活化蛋白激酶和mTOR的表达,升高了癌细胞抑制因子p53、Rb、p21和regulalcin的水平。过表达RGPR-p117可抑制癌细胞的迁移和粘附。有趣的是,与MDA-MB-231细胞共培养后,参与骨微环境的成骨细胞MC3T3-E1细胞或巨噬细胞RAW264.7细胞受损。癌细胞的作用通过转染被阻断。与从乳腺癌细胞中获得的条件培养基共培养,抑制了成骨细胞和巨噬细胞的增殖,增强了它们的死亡。TNF-α信号抑制剂阻断了这些作用。因此,我们发现过表达的RGPR-p117通过调控多种信号过程抑制乳腺癌细胞的活性,为细胞信号调控提供了新的认识。
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引用次数: 0
RETRACTION: Amp-Kinase Inhibitor Dorsomorphin Reduces the Proliferation and Migration Behavior of Colorectal Cancer Cells by Targeting the Akt/mTOR Pathway 撤回:amp激酶抑制剂Dorsomorphin通过靶向Akt/mTOR通路降低结直肠癌细胞的增殖和迁移行为。
IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2025-01-05 DOI: 10.1002/iub.2941

RETRACTION: S. Ghanaatgar-Kasbi, F. Amerizadeh, F. Rahmani, S. M. Hassanian, M. Khazaei, G. A. Ferns and A. Avan, “Amp-Kinase Inhibitor Dorsomorphin Reduces the Proliferation and Migration Behavior of Colorectal Cancer Cells by Targeting the Akt/mTOR Pathway,” IUBMB Life 71, no. 12 (2019): 1929–1936, https://doi.org/10.1002/iub.2136.

The above article, published online on 30 July 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Efstathios S. Gonos; International Union of Biochemistry and Molecular Biology; and Wiley Periodicals LLC. The retraction has been agreed following an investigation into concerns raised by a third party which revealed that the TBHP image and the Dorso 5μM image in Figure 3b contained an overlap with images published elsewhere by some of the same authors. In both instances of duplication, the images were used to represent different experimental conditions. Furthermore, the western blot in Figure 4D has been inappropriately edited and there is evidence that the bands have been spliced without clearly marking the splice sites. The authors provided an explanation and some data but this was not considered sufficient to address the concerns. As a result, the editors have lost confidence in the data presented and consider the conclusions substantially compromised. The authors disagree with the retraction.

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引用次数: 0
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