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The clinicopathologic and prognostic value of CD44 expression in patients with non-small cell lung cancer: A systematic review and meta-analysis
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-24 DOI: 10.1016/j.mcp.2025.102028
Elmira Alaei , Najma Farahani , Sima Orouei , Mina Alimohammadi , Salman Daneshi , Tahoora Mousavi , Behnaz Mahmoodieh , Afshin Taheriazam , Payman Rahimzadeh , Mehrdad Hashemi

Background

CD44 is a promising target in the prognosis and treatment of non-small cell lung cancer (NSCLC). The study deals with systematic review and meta-analysis to determine the association between CD44 overexpression and survival and clinicopathological characteristics in NSCLC patients.

Methods

We used the databases Google Scholar, Web of Science, PubMed, Scopus, EMBASE, and Cochrane to conduct a systematic search of English-language literature published up to September 2023. The eligible studies were retrieved on CD44 expression, clinicopathological characteristics in NSCLC patients, and reported survival rates. The Cochran's and Higgins I2 tests were used to measure heterogeneity across the included studies. P < 0.05 was considered statistically significant in all cases. The sources of heterogeneity across the included studies were identified using subgroup analysis on histology (SCC, ADC, and LCC), tumor differentiation (well, moderate, and poor), TMN stage (I/II/III/IV), OS, and lymph node metastasis (negative and positive). All statistical analyses were carried out using meta-analysis (CMA) software.

Results

The final analysis for prognostic significance and clinicopathological features on 3681 participants from 25 eligible studies. The pooled event rate of overexpression CD44 for overall survival in NSCLC was 38 % and was related to SCC with 76.6 %. Furthermore, subgroup analysis revealed a link between CD44 overexpression and moderate tumor differentiation (41.8 %). There was a substantial difference in CD44 overexpression in males, with 69.3 % (95 % CI: 64.3–73.9 %, I2 = 88.25 %) versus 31.5 % (95 % CI: 26.7–36.8 %, I2 = 92.15 %) in females. However, no significant relationship was observed between CD44 overexpression and TMN stages/lymph node metastasis.

Conclusion

The meta-analysis demonstrated that CD44 is an effective prognostic factor for NSCLC. Overexpression of CD44 has been linked to moderate tumor differentiation, SCC tumor histology, and a worse survival rate. However, no substantial relationship was found between CD44 and metastasis or TMN stages. Large-scale prospective research is required to validate CD44's clinical value as an unbiased prognostic indicator.
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引用次数: 0
Differential gene expression in uterine endometrioid cancer cells and adjusted normal tissue
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-14 DOI: 10.1016/j.mcp.2025.102027
Dominik Kodada , Dominik Hadžega , Patrik Krumpolec , Nikola Janoštiaková , Gabriela Bľandová , Pavol Janega , Zuzana Ballová , Erik Dosedla , Gabriel Minárik , Vanda Repiská
Endometrial cancer is a significant public health concern with rising incidence rates globally. Understanding the molecular mechanisms underlying this disease is crucial for developing effective therapeutic strategies. Our study aimed to characterize transcriptional changes in endometrial cancer tissues compared to adjusted healthy tissue. Using RNA sequencing, we identified 2483 differentially expressed genes (DEGs), including protein-coding genes, long non-coding RNAs (lncRNAs), and microRNAs (miRNAs). Notably, several known cancer-related genes were differentially expressed, such as MYC, AKT3, CCND1, and CDKN2A. Pathway analysis revealed significant alterations in cell cycle regulation, several signaling pathways, and metabolic processes. These findings provide valuable insights into the molecular pathways dysregulated in endometrial cancer. Our results may contribute to the development of novel therapeutic targets and biomarkers for this disease.
子宫内膜癌是一个重大的公共卫生问题,全球发病率不断上升。了解这种疾病的分子机制对于制定有效的治疗策略至关重要。我们的研究旨在描述子宫内膜癌组织与调整后的健康组织相比的转录变化特征。通过 RNA 测序,我们发现了 2483 个差异表达基因(DEGs),包括蛋白编码基因、长非编码 RNAs(lncRNAs)和 microRNAs(miRNAs)。值得注意的是,一些已知的癌症相关基因出现了差异表达,如 MYC、AKT3、CCND1 和 CDKN2A。通路分析表明,细胞周期调控、几种信号通路和代谢过程都发生了重大改变。这些发现为了解子宫内膜癌中失调的分子通路提供了有价值的见解。我们的研究结果可能有助于开发该疾病的新型治疗靶点和生物标记物。
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引用次数: 0
Transcriptomic analysis of intracellular RNA granules and small extracellular vesicles: Unmasking their overlap in a cell model of Huntington's disease
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-14 DOI: 10.1016/j.mcp.2025.102026
Deepti Kailash Nabariya , Lisa Maria Knüpfer , Patrick Hartwich , Manuela S. Killian , Florian Centler , Sybille Krauß
Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine protein. These aberrant RNA-protein ineractions also seed the formation of cytoplasmic liquid-like granules, such as stress granules. Emerging evidence demonstrates that granules formed via liquid-liquid phase separation can mature into gel-like inclusions that persist within the cell and may act as precursor to aggregates that occur in patients' tissue. Thus, deregulation of RNA granules is an important component of neurodegeneration. Interestingly, both the formation of intracellular membrane-less organelles like stress granules and the secretion of small extracellular vesicles (sEVs) increase upon stress and under disease conditions. sEVs are lipid membrane-bound particles that are secreted from all cell types and may participate in the spreading of misfolded proteins and aberrant RNA-protein complexes across the central nervous system in neurodegenerative diseases like HD. In this study, we performed a comparative transcriptomic analysis of sEVs and RNA granules in an HD model. RNA granules and sEVs were isolated from an inducible HD cell model. Both sEVs and RNA granules were isolated from induced (HD) and non-induced (control) cells and analyzed by RNA sequencing. Our comparative analysis between the transcriptomics data of HD RNA granules and sEVs showed that: (I) intracellular RNA granules and extracellular RNA vesicles share content, (II) several non-coding RNAs translocate to RNA granules, and (III) the composition of RNA granules and sEVs is affected in HD cells. Our data showing common transcripts in intracellular RNA granules and extracellular sEVs suggest that formation of RNA granules and sEV loading may be related. Moreover, we found a high abundance of lncRNAs in both control and HD samples, with several transcripts under REST regulation, highlighting their potential role in HD pathogenesis and selective incorporation into sEVs. The transcriptome cargo of RNA granules or sEVs may serve as a source for diagnostic strategies. For example, disease-specific RNA-signatures of sEVs can serve as biomarker of central nervous system diseases. Therefore, we compared our dataset to transcriptomic data from HD patient sEVs in blood. However, our data suggest that the cell-type specific signature of sEV-secreted RNAs as well as their high variability may make it difficult to detect these biomarkers in blood.
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引用次数: 0
BUB1-deficiency suppresses kidney renal clear cell carcinoma progression via the PI3K/Akt pathway: A bioinformatics-oriented validating study
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-11 DOI: 10.1016/j.mcp.2025.102024
Xiaolin Zi , Jinpeng Ma , Xiaoxia Li , Honglei Wang , Yuchen Bao , Tao Deng , Xueli Yuan
Although great advances have been reached in the diagnosis, treatment and prognosis of kidney renal clear cell carcinoma (KIRC), the advancement of therapeutic strategies for KIRC in clinical practices have been seriously limited due to its unknown molecular mechanisms. To resolve this issue, through analyzing the datasets from the online UCSC database, a novel BUB1 gene was found to be elevated in the cancerous tissues compared to their normal tissues of KIRC, and and KIRC patients with high-expressed BUB1 tended to have a worse prognosis. The subsequent experiments validated that BUB1 protein was located in both nucleus and cytoplasm of KIRC cells, and the expression levels of BUB1 gene were significantly elevated in KIRC tissues and cells, in contrast to their normal counterparts. Loss-of-function experiments verified that knockdown of BUB1 suppressed cell proliferation, mobility, epithelial-mesenchymal transition (EMT) and tumor growth, whereas induced apoptotic cell death in the KIRC cells in vitro and in vivo. In addition, bioinformatics analysis predicted that the differentially-expressed genes (DEGs) in the BUB1-deficient cohorts were enriched in the cell division-related PI3K/Akt signal pathway, and we evidenced that silencing of BUB1 was capable of inactivating the downstream PI3K/Akt signal pathway. Of note, deficiency of BUB1-induced suppressing effects on the malignant phenotypes in KIRC cells were all reversed by co-treating cells with PI3K/Akt pathway activator 740Y-P. Furthermore, it was found that the expression status of BUB1 gene were related with epigenetic modifications, immune infiltration and immunotherapy responses in KIRC. Collectively, silencing of BUB1 inhibited the progression of KIRC through inactivating the downstream PI3K/Akt signal pathway, and BUB1 gene could be potentially used as biomarkers for the diagnosis and treatment of KIRC in clinic.
{"title":"BUB1-deficiency suppresses kidney renal clear cell carcinoma progression via the PI3K/Akt pathway: A bioinformatics-oriented validating study","authors":"Xiaolin Zi ,&nbsp;Jinpeng Ma ,&nbsp;Xiaoxia Li ,&nbsp;Honglei Wang ,&nbsp;Yuchen Bao ,&nbsp;Tao Deng ,&nbsp;Xueli Yuan","doi":"10.1016/j.mcp.2025.102024","DOIUrl":"10.1016/j.mcp.2025.102024","url":null,"abstract":"<div><div>Although great advances have been reached in the diagnosis, treatment and prognosis of kidney renal clear cell carcinoma (KIRC), the advancement of therapeutic strategies for KIRC in clinical practices have been seriously limited due to its unknown molecular mechanisms. To resolve this issue, through analyzing the datasets from the online UCSC database, a novel BUB1 gene was found to be elevated in the cancerous tissues compared to their normal tissues of KIRC, and and KIRC patients with high-expressed BUB1 tended to have a worse prognosis. The subsequent experiments validated that BUB1 protein was located in both nucleus and cytoplasm of KIRC cells, and the expression levels of BUB1 gene were significantly elevated in KIRC tissues and cells, in contrast to their normal counterparts. Loss-of-function experiments verified that knockdown of BUB1 suppressed cell proliferation, mobility, epithelial-mesenchymal transition (EMT) and tumor growth, whereas induced apoptotic cell death in the KIRC cells <em>in vitro</em> and <em>in vivo</em>. In addition, bioinformatics analysis predicted that the differentially-expressed genes (DEGs) in the BUB1-deficient cohorts were enriched in the cell division-related PI3K/Akt signal pathway, and we evidenced that silencing of BUB1 was capable of inactivating the downstream PI3K/Akt signal pathway. Of note, deficiency of BUB1-induced suppressing effects on the malignant phenotypes in KIRC cells were all reversed by co-treating cells with PI3K/Akt pathway activator 740Y-P. Furthermore, it was found that the expression status of BUB1 gene were related with epigenetic modifications, immune infiltration and immunotherapy responses in KIRC. Collectively, silencing of BUB1 inhibited the progression of KIRC through inactivating the downstream PI3K/Akt signal pathway, and BUB1 gene could be potentially used as biomarkers for the diagnosis and treatment of KIRC in clinic.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"81 ","pages":"Article 102024"},"PeriodicalIF":2.3,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143626545","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
Down-regulated circ_0001853 inhibits lipopolysaccharide-induced endometritis progression via sponging miR-34c-5p
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-07 DOI: 10.1016/j.mcp.2025.102023
Qian Xu, Ailing Peng, Liyun Zhao, Li Wang

Background

To investigate the diagnostic value and mechanism of action of circular RNA (circ_) circ_0001853 and microRNA (miR) miR-34c-5p in patients with endometritis.

Methods

189 patients with endometritis and 176 healthy individuals were included in this study. Venous blood serum was collected from the study subjects and stored temporarily at −80 °C. Real-time quantitative chain polymerase reaction (RT-qPCR) was used to detect circ_0001853 and miR-34c-5p expression, and receiver operating characteristic (ROC) curves assessed the diagnostic value of both in predicting endometritis. Cell counting kit (CCK8) observed cell proliferation, flow cytometry recorded apoptosis, enzyme linked immunosorbent assay (ELISA) monitored inflammatory factor expression, and dual luciferase reporter assay and RNA immunoprecipitation (RIP) verified the relationship between circ_0001853 and miR-34c-5p targeting interactions.

Results

High levels of circ_0001853 and low levels of miR-34c-5p were present in endometritis patients, and they were negatively correlated. Both circ_0001853 and miR-34c-5p alone or in combination had diagnostic value in predicting the progression of endometritis. Transfection of si-circ_0001853 promoted cell proliferation and reduced apoptosis and cellular inflammation levels induced by lipopolysaccharide (LPS) stimulation. There was a direct reciprocal targeting relationship between miR-34c-5p and circ_0001853, and the use of miR-34c-5p inhibitor resisted silencing circ_0001853 promoted cell proliferation and increased the number of apoptotic cells and cellular inflammation levels.

Conclusions

circ_0001853 is involved in endometritis progression through miR-34c-5p, i.e., low circ_0001853 promotes miR-34c-5p-induced proliferation of epithelial cells, reduces apoptosis, and suppresses inflammation levels, preventing disease progression.
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引用次数: 0
Corrigendum to “Identification of circRNA-mediated competing endogenous RNA network involved in the development of cervical cancer” [Mol. Cell. Probes. 78 (2024) 101984]
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-07 DOI: 10.1016/j.mcp.2025.102021
Shaosheng Lou , Wang Yang , Qian Zhao , Yunshan Ouyang , Lingling Cao , Chen Lin
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引用次数: 0
Silymarin plus doxorubicin exerts the anti-hepatocellular carcinoma effects via Wnt, apoptosis, autophagy and angiogenesis pathways
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-04 DOI: 10.1016/j.mcp.2025.102022
Baohong Yuan , Ruotian Wang , Zehai Gao , Hameed Mirzeei , An-Dong Xiang , Feng Guo

Background

The biggest cause of death worldwide is liver cancer. Despite several initiatives and successes in treatment techniques, only a little improvement has been attained. In order to control this cancer, new therapeutic strategies are therefore required. Here, we evaluated the effects of doxorubicin and the milk thistle plant phytochemical Silymarin on liver cancer through apoptosis, autophagy, and Wnt signaling.

Methods

Silymarin both alone and together with doxorubicin was administered to induce cytotoxicity in the H22 cell line. qRT-PCR and Western blot analyses, the genes related to autophagy, Wnt signals, and cell death were examined.

Results

Doxorubicin and Silymarin both individually and combined dramatically slowed down H22 cells growth. Additionally, there was a significant drop in the Bcl-2 protein and a considerable rise in the caspase 8 and Bax proteins. LC3-I, LC3-II, and Beclin 1 have been all shown to be significantly elevated. Moreover, there was a substantial decrease in the expression of genes involved in the Wnt pathway, including cyclin D1, β-catenin, ZEB1, and Twist. The levels of AMPK were decreased in Silymarin with Doxorubicin alone and in combination, whereas VASP, VEGF, and HIF-1a were lowest.

Conclusion

Silymarin may enhance anti-tumor effects of doxorubicin through modulating autophagy, angiogenesis, and apoptosis, in-vitro.
{"title":"Silymarin plus doxorubicin exerts the anti-hepatocellular carcinoma effects via Wnt, apoptosis, autophagy and angiogenesis pathways","authors":"Baohong Yuan ,&nbsp;Ruotian Wang ,&nbsp;Zehai Gao ,&nbsp;Hameed Mirzeei ,&nbsp;An-Dong Xiang ,&nbsp;Feng Guo","doi":"10.1016/j.mcp.2025.102022","DOIUrl":"10.1016/j.mcp.2025.102022","url":null,"abstract":"<div><h3>Background</h3><div>The biggest cause of death worldwide is liver cancer. Despite several initiatives and successes in treatment techniques, only a little improvement has been attained. In order to control this cancer, new therapeutic strategies are therefore required. Here, we evaluated the effects of doxorubicin and the milk thistle plant phytochemical Silymarin on liver cancer through apoptosis, autophagy, and Wnt signaling.</div></div><div><h3>Methods</h3><div>Silymarin both alone and together with doxorubicin was administered to induce cytotoxicity in the H22 cell line. qRT-PCR and Western blot analyses, the genes related to autophagy, Wnt signals, and cell death were examined.</div></div><div><h3>Results</h3><div>Doxorubicin and Silymarin both individually and combined dramatically slowed down H22 cells growth. Additionally, there was a significant drop in the Bcl-2 protein and a considerable rise in the caspase 8 and Bax proteins. LC3-I, LC3-II, and Beclin 1 have been all shown to be significantly elevated. Moreover, there was a substantial decrease in the expression of genes involved in the Wnt pathway, including cyclin D1, β-catenin, ZEB1, and Twist. The levels of AMPK were decreased in Silymarin with Doxorubicin alone and in combination, whereas VASP, VEGF, and HIF-1a were lowest.</div></div><div><h3>Conclusion</h3><div>Silymarin may enhance anti-tumor effects of doxorubicin through modulating autophagy, angiogenesis, and apoptosis, <em>in-vitro</em>.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"81 ","pages":"Article 102022"},"PeriodicalIF":2.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143574471","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
Clinical value of microRNA-4449 of non-small cell lung cancer patients undergoing thoracic paravertebral block thoracotomy
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-03-01 DOI: 10.1016/j.mcp.2025.102020
Yu Sun , Jiantao Zhang , Licai Zhang , Liquan Qiu , Huayi Zhang

Objective

The aim of this study was to investigate the clinical significance of microRNA-4449 (miR-4449) in patients attacked by non-small cell lung cancer (NSCLC) undergoing thoracic paravertebral block (TPVB) thoracotomy.

Methods

A total of 122 patients diagnosed with NSCLC and 101 healthy individuals were recruited in this case-control study. Quantitative real-time polymerase reaction time (qRT-PCR) assay was applied to quantify the serum levels of miR-4449 in all participants. To assess the diagnostic potential of miR-4449, receiver operating characteristic (ROC) curves were constructed. Additionally, the prognostic value of miR-4449 was evaluated using Kaplan-Meier method and Cox regression analyses. The possible target genes and related proteins of miR-4449 were predicted via bioinformatics analysis.

Results

MiR-4449 expression was notably reduced in NSCLC patients relative to healthy volunteers (P < 0.001), with the area under the curve (AUC) reaching 0.952, demonstrating its ability to effectively differentiate between NSCLC patients and healthy individuals. Serum levels of miR-4449 were negatively in relation to tumor node metastasis stage and lymph node metastasis (P < 0.05). Moreover, a significant increase in miR-4449 expression was observed in patients following TPVB thoracotomy, as compared to pre-operative levels (P < 0.001). The AUC of 0.884 further highlighted its potential to distinguish between the effective group and the invalid group. Notably, patients expressing high levels of miR-4449 exhibited improved overall survival (P < 0.001), and miR-4449 (P < 0.001, HR = 2.290, 95 % = 1.450–3.615) was identified as an independently prognostic predictor for NSCLC. Bioinformatics analysis of miR-4999 target genes revealed key tumor-associated pathways and proteins, offering valuable insights into its molecular mechanisms in NSCLC.

Conclusion

Serum levels of miR-4449 were significantly decreased in patients with NSCLC and exhibited a correlation with the severity of the tumor. Furthermore, miR-4449 emerged as a potential prognostic biomarker, offering valuable insight into the clinical outcome for NSCLC undergoing TPVB thoracotomy.
研究目的本研究旨在探讨接受胸椎旁阻滞(TPVB)开胸手术的非小细胞肺癌(NSCLC)患者体内microRNA-4449(miR-4449)的临床意义:这项病例对照研究共招募了 122 名确诊为 NSCLC 的患者和 101 名健康人。采用实时定量聚合酶反应时间(qRT-PCR)测定所有参与者血清中的 miR-4449 水平。为了评估 miR-4449 的诊断潜力,研究人员绘制了接收者操作特征曲线(ROC)。此外,还使用 Kaplan-Meier 法和 Cox 回归分析评估了 miR-4449 的预后价值。通过生物信息学分析预测了miR-4449可能的靶基因和相关蛋白:结果:与健康志愿者相比,NSCLC 患者的 miR-4449 表达明显降低(PC结论:血清中 miR-4449 的水平在 NSCLC 患者中明显降低:NSCLC患者血清中的miR-4449水平明显下降,并与疾病的严重程度相关。此外,miR-4449还是一种潜在的预后生物标志物,为了解接受TPVB开胸手术的NSCLC患者的临床预后提供了有价值的信息。
{"title":"Clinical value of microRNA-4449 of non-small cell lung cancer patients undergoing thoracic paravertebral block thoracotomy","authors":"Yu Sun ,&nbsp;Jiantao Zhang ,&nbsp;Licai Zhang ,&nbsp;Liquan Qiu ,&nbsp;Huayi Zhang","doi":"10.1016/j.mcp.2025.102020","DOIUrl":"10.1016/j.mcp.2025.102020","url":null,"abstract":"<div><h3>Objective</h3><div>The aim of this study was to investigate the clinical significance of microRNA-4449 (miR-4449) in patients attacked by non-small cell lung cancer (NSCLC) undergoing thoracic paravertebral block (TPVB) thoracotomy.</div></div><div><h3>Methods</h3><div>A total of 122 patients diagnosed with NSCLC and 101 healthy individuals were recruited in this case-control study. Quantitative real-time polymerase reaction time (qRT-PCR) assay was applied to quantify the serum levels of miR-4449 in all participants. To assess the diagnostic potential of miR-4449, receiver operating characteristic (ROC) curves were constructed. Additionally, the prognostic value of miR-4449 was evaluated using Kaplan-Meier method and Cox regression analyses. The possible target genes and related proteins of miR-4449 were predicted via bioinformatics analysis.</div></div><div><h3>Results</h3><div>MiR-4449 expression was notably reduced in NSCLC patients relative to healthy volunteers (<em>P</em> &lt; 0.001), with the area under the curve (AUC) reaching 0.952, demonstrating its ability to effectively differentiate between NSCLC patients and healthy individuals. Serum levels of miR-4449 were negatively in relation to tumor node metastasis stage and lymph node metastasis (<em>P</em> &lt; 0.05). Moreover, a significant increase in miR-4449 expression was observed in patients following TPVB thoracotomy, as compared to pre-operative levels (<em>P</em> &lt; 0.001). The AUC of 0.884 further highlighted its potential to distinguish between the effective group and the invalid group. Notably, patients expressing high levels of miR-4449 exhibited improved overall survival (<em>P</em> &lt; 0.001), and miR-4449 (<em>P</em> &lt; 0.001, HR = 2.290, 95 % = 1.450–3.615) was identified as an independently prognostic predictor for NSCLC. Bioinformatics analysis of miR-4999 target genes revealed key tumor-associated pathways and proteins, offering valuable insights into its molecular mechanisms in NSCLC.</div></div><div><h3>Conclusion</h3><div>Serum levels of miR-4449 were significantly decreased in patients with NSCLC and exhibited a correlation with the severity of the tumor. Furthermore, miR-4449 emerged as a potential prognostic biomarker, offering valuable insight into the clinical outcome for NSCLC undergoing TPVB thoracotomy.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102020"},"PeriodicalIF":2.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143473049","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
Serum exosomal miR-454-3p contributes to malignant progression of lung cancer by inhibiting HHEX
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-16 DOI: 10.1016/j.mcp.2025.102019
Gangqin Hu, Peng Cai, Jingjing Li, Liuyang Yu, Bolin Zhao, Guiming Chen

Background

Lung cancer is a common cancer. Exosomes are emerging mediators of intercellular communication, and miRNAs serve a crucial position in cancer progression. This project intends to discover whether exosomal miR-454-3p affects tumor progression and its underlying mechanisms.

Methods

Exosomes were isolated utilizing ultracentrifugation. The exosomal biomarkers level was monitored by western blot (WB). The miR-454-3p levels were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and HHEX expression were detected by qRT-PCR and WB. Cell growth and metastasis were detected through CCK-8, colony formation assay and transwell. Meanwhile, the dual luciferase reporter system and immunoprecipitation (RIP) assay was applied to clarify the interactions between miR-454-3p and HHEX.

Results

We successfully isolated serum exosomes from NSCLC patients. Then, our team discovered that miR-454-3p was elevated in serum-derived exosomes from NSCLC patients. Functional analysis disclosed that exosomes accelerated NSCLC cell proliferation and metastasis. Silencing of exosomal miR-454-3p hindered NSCLC cell proliferation and metastasis. Subsequently, the starbase database declared that miR-454-3p was interacted with HHEX. HHEX overexpression reversed the promotion of NSCLC cell proliferation and metastasis by exosomal miR-454-3p.

Conclusions

Exosomal miR-454-3p enhanced the progression of NSCLC cells through HHEX. miR-454-3p may be a therapeutic target for NSCLC.
{"title":"Serum exosomal miR-454-3p contributes to malignant progression of lung cancer by inhibiting HHEX","authors":"Gangqin Hu,&nbsp;Peng Cai,&nbsp;Jingjing Li,&nbsp;Liuyang Yu,&nbsp;Bolin Zhao,&nbsp;Guiming Chen","doi":"10.1016/j.mcp.2025.102019","DOIUrl":"10.1016/j.mcp.2025.102019","url":null,"abstract":"<div><h3>Background</h3><div>Lung cancer is a common cancer. Exosomes are emerging mediators of intercellular communication, and miRNAs serve a crucial position in cancer progression. This project intends to discover whether exosomal miR-454-3p affects tumor progression and its underlying mechanisms.</div></div><div><h3>Methods</h3><div>Exosomes were isolated utilizing ultracentrifugation. The exosomal biomarkers level was monitored by western blot (WB). The miR-454-3p levels were assessed by quantitative reverse transcription polymerase chain reaction (qRT-PCR), and HHEX expression were detected by qRT-PCR and WB. Cell growth and metastasis were detected through CCK-8, colony formation assay and transwell. Meanwhile, the dual luciferase reporter system and immunoprecipitation (RIP) assay was applied to clarify the interactions between miR-454-3p and HHEX.</div></div><div><h3>Results</h3><div>We successfully isolated serum exosomes from NSCLC patients. Then, our team discovered that miR-454-3p was elevated in serum-derived exosomes from NSCLC patients. Functional analysis disclosed that exosomes accelerated NSCLC cell proliferation and metastasis. Silencing of exosomal miR-454-3p hindered NSCLC cell proliferation and metastasis. Subsequently, the starbase database declared that miR-454-3p was interacted with HHEX. HHEX overexpression reversed the promotion of NSCLC cell proliferation and metastasis by exosomal miR-454-3p.</div></div><div><h3>Conclusions</h3><div>Exosomal miR-454-3p enhanced the progression of NSCLC cells through HHEX. miR-454-3p may be a therapeutic target for NSCLC.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102019"},"PeriodicalIF":2.3,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143392333","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
The role of APOA1-AS in colorectal cancer: Investigating its association with malignant biological behaviors APOA1-AS 在结直肠癌中的作用:研究其与恶性生物学行为的关系
IF 2.3 3区 生物学 Q3 BIOCHEMICAL RESEARCH METHODS Pub Date : 2025-02-16 DOI: 10.1016/j.mcp.2025.102017
Gang Liu , Qin Zhao , Yan Li , Dongmei Zhu , Hong Peng

Purpose

Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms.

Methods

Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed.

Results

A total of 2985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway.

Conclusion

Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.
{"title":"The role of APOA1-AS in colorectal cancer: Investigating its association with malignant biological behaviors","authors":"Gang Liu ,&nbsp;Qin Zhao ,&nbsp;Yan Li ,&nbsp;Dongmei Zhu ,&nbsp;Hong Peng","doi":"10.1016/j.mcp.2025.102017","DOIUrl":"10.1016/j.mcp.2025.102017","url":null,"abstract":"<div><h3>Purpose</h3><div>Colorectal cancer (CRC) is a common malignant tumor associated with high morbidity and mortality. Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression. This study aimed to explore the role of lncRNA APOA1-AS in colorectal cancer and elucidate its underlying mechanisms.</div></div><div><h3>Methods</h3><div>Clinical samples were collected, and high-throughput sequencing was performed to identify differentially expressed lncRNAs in colorectal cancer. Among these, the key lncRNA APOA1-AS was selected for further investigation. The expression of APOA1-AS in colorectal cancer tissues and cells was evaluated. The effects of APOA1-AS on cell proliferation, migration, invasion, and apoptosis were assessed through knockdown and overexpression of APOA1-AS in SW620 and RKO cells. Additionally, the relationship between APOA1-AS and the malignant biological behaviors of colorectal cancer cells was also investigated. Furthermore, the involvement of APOA1-AS in glucose metabolism reprogramming and the cGMP-PKG signaling pathway was analyzed.</div></div><div><h3>Results</h3><div>A total of 2985 differentially expressed lncRNAs were identified in colorectal cancer, including APOA1-AS, which showed the most significant upregulation. APOA1-AS expression was significantly higher in colorectal cancer tissues compared to normal tissues. Overexpression of APOA1-AS promoted cell proliferation, migration, and invasion while inhibiting apoptosis in SW620 and RKO cells. Furthermore, APOA1-AS was found to regulate glucose metabolism reprogramming, enhance tumor malignant biological behaviors and facilitate tumor cell drug resistance through the cGMP-PKG signaling pathway.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates that APOA1-AS is a potential key regulator in colorectal cancer development and progression. It functions via glucose metabolism reprogramming and the cGMP-PKG signaling pathway, offering a novel therapeutic target for colorectal cancer.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"80 ","pages":"Article 102017"},"PeriodicalIF":2.3,"publicationDate":"2025-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076122","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
期刊
Molecular and Cellular Probes
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