Pub Date : 2024-05-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024050357
Chhaya Pandey, Prakash Tiwari
MicroRNAs are short non-coding RNAs that inhibit gene expression at the post-transcriptional level. Abnormal microRNA expression has been associated with different human diseases, including cancer. Epigenetic changes, mutation, transcriptional deregulation, DNA copy number abnormalities, and defects in the biogenesis machinery play an important role in abnormal microRNA expression. Modulation of micro RNAs by natural agents has emerged to enhance the efficacy of conventional chemotherapy through combinatorial therapeutic approach. This review summarizes the current understanding of abnormal microRNA expression in cancer, the different cellular mechanisms of microRNA, and their prevention by natural compounds. Understanding microRNA expression patterns during cancer development may help to identify stage-specific molecular markers. Natural compounds that exert regulatory effects by modulating microRNAs can be used in better cancer chemopreventive strategies by directly targeting microRNAs or as a way to increase sensitivity to existing chemotherapy regimens.
{"title":"Differential microRNAs expression during cancer development, and chemoprevention by natural compounds: a comprehensive review.","authors":"Chhaya Pandey, Prakash Tiwari","doi":"10.1615/jenvironpatholtoxicoloncol.2024050357","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024050357","url":null,"abstract":"MicroRNAs are short non-coding RNAs that inhibit gene expression at the post-transcriptional level. Abnormal microRNA expression has been associated with different human diseases, including cancer. Epigenetic changes, mutation, transcriptional deregulation, DNA copy number abnormalities, and defects in the biogenesis machinery play an important role in abnormal microRNA expression. Modulation of micro RNAs by natural agents has emerged to enhance the efficacy of conventional chemotherapy through combinatorial therapeutic approach. This review summarizes the current understanding of abnormal microRNA expression in cancer, the different cellular mechanisms of microRNA, and their prevention by natural compounds. Understanding microRNA expression patterns during cancer development may help to identify stage-specific molecular markers. Natural compounds that exert regulatory effects by modulating microRNAs can be used in better cancer chemopreventive strategies by directly targeting microRNAs or as a way to increase sensitivity to existing chemotherapy regimens.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"25 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140831304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024053394
Qi Zhao, Shi Xiong, Hourong Cai, Xiaofeng He
Background: As one of the three major malignant tumors, LUAD, with its rapid progression and high mortality rate, has become the most dangerous factor endangering human health. Objectives: To find new therapeutic targets to improve the early diagnosis and prognosis of LUAD. This study conducted related experiments to explore the expression and function of LncRNA APTR in LUAD. Materials and methods: The expression of APTR in LUAD was detected by PCR experiments, and the relationship between APTR and patients' clinical conditions and prognosis was analyzed by Chi-square test, multifactor Cox regression, and Kaplan-Meier. The interaction between APTR and miR-298 and the regulation of LUAD cellular activities by APTR/miR-298 were explored by the Luciferase reporter gene system. Results: APTR expression was found to be upregulated in LUAD tissues and cells, and the expression of APTR was revealed to be substantially linked with lymph node metastases and TNM stage. High expression of LUAD also predicted a poor prognosis for patients. Down-regulation of APTR expression significantly inhibited the activities of LUAD cells. In addition, APTR targeted miR-298 and negatively regulated miR-298 expression. The inhibitory effect of APTR knockdown on LUAD cell activity was also reversed after transfection with miR-298 inhibitor. Conclusions: Increasing expression of APTR is associated with patients’ poor prognosis, APTR targets miR-298 and promotes LUAD cellular activity through negative regulation of miR-298.
{"title":"Expression and significance of LncRNA APTR in the occurrence and development of LUAD","authors":"Qi Zhao, Shi Xiong, Hourong Cai, Xiaofeng He","doi":"10.1615/jenvironpatholtoxicoloncol.2024053394","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053394","url":null,"abstract":"Background: As one of the three major malignant tumors, LUAD, with its rapid progression and high mortality rate, has become the most dangerous factor endangering human health.\u0000Objectives: To find new therapeutic targets to improve the early diagnosis and prognosis of LUAD. This study conducted related experiments to explore the expression and function of LncRNA APTR in LUAD.\u0000Materials and methods: The expression of APTR in LUAD was detected by PCR experiments, and the relationship between APTR and patients' clinical conditions and prognosis was analyzed by Chi-square test, multifactor Cox regression, and Kaplan-Meier. The interaction between APTR and miR-298 and the regulation of LUAD cellular activities by APTR/miR-298 were explored by the Luciferase reporter gene system.\u0000Results: APTR expression was found to be upregulated in LUAD tissues and cells, and the expression of APTR was revealed to be substantially linked with lymph node metastases and TNM stage. High expression of LUAD also predicted a poor prognosis for patients. Down-regulation of APTR expression significantly inhibited the activities of LUAD cells. In addition, APTR targeted miR-298 and negatively regulated miR-298 expression. The inhibitory effect of APTR knockdown on LUAD cell activity was also reversed after transfection with miR-298 inhibitor.\u0000Conclusions: Increasing expression of APTR is associated with patients’ poor prognosis, APTR targets miR-298 and promotes LUAD cellular activity through negative regulation of miR-298.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"30 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140940435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-05-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024053229
Zhuo Chen, Shengnan Liu, Junsheng Wang, Yang Chen
Background: Acute pancreatitis (AP) is a common digestive emergency, requiring early prediction and recognition. The study examined the clinical value of long non-coding RNA SNHG1 in AP, and explored its related mechanism for AP. Methods: A total of 288 AP patients were grouped based on AP severity. AR42J cells were treated with 100nM caerulein to stimulate AP in vitro, and the cell viability and apoptosis were tested. qRT-PCR was performed for mRNA detection. Logistic regression analysis was done to identify influence factors. Receiver operating characteristic (ROC) curve was generated for diagnostic value evaluation. The targets of SNHG1 or miR-140-3p were predicted using online prediction tolls, and were verified via luciferase reporter and RNA immunoprecipitation (RIP) assay. Results: High expression levels of SNHG1 were detected in the serum of AP patients, and it can differentiate AP cases from healthy people with the AUC of 0.899. Severe AP cases had high values of SNHG1, which was independently related to AP severity. SNHG1 knockdown relieved caerulein-induced AR42J cell apoptosis and inflammatory response. MiR-140-3p interacted with SNHG1, and reversed the role of SNHG1 in caerulein-induced AR42J cell injury. RAB21 was a candidate target gene of miR-140-3p, and was at high expression in AP cell models. Conclusion: SNHG1 may be a promising biomarker for the detection of AP, and serves as a potential biological marker for further risk stratification in the management of AP. SNHG1 knockdown can relieve inflammatory responses and pancreatic cell apoptosis by absorbing miR-140-3p.
背景：急性胰腺炎（AP）是一种常见的消化系统急症，需要早期预测和识别。本研究探讨了长非编码 RNA SNHG1 在急性胰腺炎中的临床价值，并探讨了其与急性胰腺炎的相关机制：方法：根据 AP 严重程度对 288 例 AP 患者进行分组。用 100nM caerulein 处理 AR42J 细胞以体外刺激 AP，检测细胞活力和凋亡。进行逻辑回归分析以确定影响因素。生成接收者操作特征曲线（ROC）用于诊断价值评估。利用在线预测工具预测了SNHG1或miR-140-3p的靶点，并通过荧光素酶报告和RNA免疫沉淀（RIP）实验进行了验证：结果：在 AP 患者血清中检测到 SNHG1 的高表达水平，其 AUC 为 0.899，可将 AP 病例与健康人群区分开来。重症AP病例的SNHG1表达量较高，且与AP的严重程度独立相关。敲除SNHG1可以缓解caerulein诱导的AR42J细胞凋亡和炎症反应。MiR-140-3p与SNHG1相互作用，逆转了SNHG1在caerulein诱导的AR42J细胞损伤中的作用。RAB21是miR-140-3p的候选靶基因，并且在AP细胞模型中高表达：结论：SNHG1可能是一种很有前景的检测AP的生物标志物，也是一种潜在的生物标志物，可用于AP治疗中的进一步风险分层。SNHG1敲除可通过吸收miR-140-3p缓解炎症反应和胰腺细胞凋亡。
{"title":"Long non-coding RNA SNHG1 predicts disease severity of acute pancreatitis and stimulates pancreatic cell apoptosis and inflammatory response","authors":"Zhuo Chen, Shengnan Liu, Junsheng Wang, Yang Chen","doi":"10.1615/jenvironpatholtoxicoloncol.2024053229","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053229","url":null,"abstract":"Background: Acute pancreatitis (AP) is a common digestive emergency, requiring early prediction and recognition. The study examined the clinical value of long non-coding RNA SNHG1 in AP, and explored its related mechanism for AP.\u0000Methods: A total of 288 AP patients were grouped based on AP severity. AR42J cells were treated with 100nM caerulein to stimulate AP in vitro, and the cell viability and apoptosis were tested. qRT-PCR was performed for mRNA detection. Logistic regression analysis was done to identify influence factors. Receiver operating characteristic (ROC) curve was generated for diagnostic value evaluation. The targets of SNHG1 or miR-140-3p were predicted using online prediction tolls, and were verified via luciferase reporter and RNA immunoprecipitation (RIP) assay.\u0000Results: High expression levels of SNHG1 were detected in the serum of AP patients, and it can differentiate AP cases from healthy people with the AUC of 0.899. Severe AP cases had high values of SNHG1, which was independently related to AP severity. SNHG1 knockdown relieved caerulein-induced AR42J cell apoptosis and inflammatory response. MiR-140-3p interacted with SNHG1, and reversed the role of SNHG1 in caerulein-induced AR42J cell injury. RAB21 was a candidate target gene of miR-140-3p, and was at high expression in AP cell models.\u0000Conclusion: SNHG1 may be a promising biomarker for the detection of AP, and serves as a potential biological marker for further risk stratification in the management of AP. SNHG1 knockdown can relieve inflammatory responses and pancreatic cell apoptosis by absorbing miR-140-3p.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"76 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140940454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024049848
Wuhan Zhou, Liang Lin, Dongxing Chen, Jiafei Chen
Background: IFN-γ exerts anti-tumor effects, but there is currently no reliable and comprehensive study on the predictive function of IFN-γ-related genes in liver cancer. Methods: In this study, IFN-γ-related differentially expressed genes (DEGs) in liver cancer were obtained through GO/KEGG databases and open-access literature. Based on these genes, liver cancer individuals were clustered. A liver cancer prognostic model was built based on the intersection genes between differential genes in clusters and in liver cancer. Then, the predictive accuracy of the model was analyzed and validated in the GEO dataset. Regression analysis was fulfilled on the model, and a nomogram was used to evaluate the ability of the model as an independent prognostic factor and its clinical application value. An immune-related analysis was conducted on both the H- and L-groups, with an additional investigation into the correlation between model genes and drug sensitivity. Results: Significant differential expression of IFN-γ-related genes was observed between the liver cancer and control groups. Subsequently, liver cancer individuals were classified into two subtypes based on these genes, which displayed a notable difference in survival between the two subtypes. A 10-gene liver cancer prognostic model was constructed, with good predictive accuracy and was an independent prognostic indicator for patient analysis. L-group patients possessed higher immune infiltration levels, immune checkpoint expression levels, and immunophenoscore, as well as lower TIDE scores. Drugs that had high correlations with the feature genes included SPANXB1: PF-04217903, SGX-523, MMP1: PF-04217903, DUSP13: Imat
背景：IFN-γ具有抗肿瘤作用，但目前还没有关于IFN-γ相关基因在肝癌中的预测功能的可靠而全面的研究：方法：本研究通过 GO/KEGG 数据库和开放获取的文献获得了肝癌中 IFN-γ 相关的差异表达基因（DEGs）。根据这些基因对肝癌个体进行聚类。根据聚类中差异基因与肝癌中差异基因之间的交叉基因，建立了肝癌预后模型。然后，在 GEO 数据集中分析并验证了该模型的预测准确性。对模型进行了回归分析，并使用提名图评估了模型作为独立预后因素的能力及其临床应用价值。对 H 组和 L 组进行了免疫相关分析，并对模型基因与药物敏感性之间的相关性进行了额外调查：结果：在肝癌组和对照组之间观察到了 IFN-γ 相关基因的显著差异表达。随后，根据这些基因将肝癌患者分为两个亚型，两个亚型之间的生存率存在明显差异。构建的 10 基因肝癌预后模型具有良好的预测准确性，是分析患者预后的独立指标。L组患者的免疫浸润水平、免疫检查点表达水平和免疫表观评分较高，TIDE评分较低。与特征基因高度相关的药物包括 SPANXB1：PF-04217903、SGX-523、MMP1：PF-04217903、DUSP13：Imat
{"title":"Construction of a liver cancer prognostic model based on IFN-γ-related genes for revealing the immune landscape and predicting drugs","authors":"Wuhan Zhou, Liang Lin, Dongxing Chen, Jiafei Chen","doi":"10.1615/jenvironpatholtoxicoloncol.2024049848","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024049848","url":null,"abstract":"Background: IFN-γ exerts anti-tumor effects, but there is currently no reliable and comprehensive study on the predictive function of IFN-γ-related genes in liver cancer.\u0000Methods: In this study, IFN-γ-related differentially expressed genes (DEGs) in liver cancer were obtained through GO/KEGG databases and open-access literature. Based on these genes, liver cancer individuals were clustered. A liver cancer prognostic model was built based on the intersection genes between differential genes in clusters and in liver cancer. Then, the predictive accuracy of the model was analyzed and validated in the GEO dataset. Regression analysis was fulfilled on the model, and a nomogram was used to evaluate the ability of the model as an independent prognostic factor and its clinical application value. An immune-related analysis was conducted on both the H- and L-groups, with an additional investigation into the correlation between model genes and drug sensitivity.\u0000Results: Significant differential expression of IFN-γ-related genes was observed between the liver cancer and control groups. Subsequently, liver cancer individuals were classified into two subtypes based on these genes, which displayed a notable difference in survival between the two subtypes. A 10-gene liver cancer prognostic model was constructed, with good predictive accuracy and was an independent prognostic indicator for patient analysis. L-group patients possessed higher immune infiltration levels, immune checkpoint expression levels, and immunophenoscore, as well as lower TIDE scores. Drugs that had high correlations with the feature genes included SPANXB1: PF-04217903, SGX-523, MMP1: PF-04217903, DUSP13: Imat","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"12 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140800693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gastric cancer, a prevalent malady within the digestive tract, has a complex pathological mechanism and numerous patients. The regulation of gastric cancer process by long non-coding RNA (lncRNA) has laid a new exploration idea for the study of its molecular mechanism and the treatment of patients. The abnormal expressed genes in gastric cancer were screened by GSE193109 dataset. The correlation between LINC01278 and the likelihood of survival in patients suffering from gastric cancer was investigated by Kaplan-Meier survival curve and multivariate Cox analysis. LINC01278 in gastric cancer tissue samples and cells was verified via RT-qPCR. The CCK-8 and Transwell assay were selected to detect the growth activity of gastric cancer cells. The association between LINC01278 and miR-129-5p was validated through luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay. Correlation analysis of clinical features revealed an association between LINC01278 and the prognosis in gastric cancer patients. LINC01278 was actively expressed in gastric cancer, which exerts a tumor-promoting effect. Silencing LINC01278 suppressed the biological function of tumor cells through spongiform miR-129-5p. LINC01278 has the potential to serve as a novel biomarker, offering new avenues of research for the prognosis and treatment of gastric cancer.
{"title":"LncRNA LINC01278 regulates the prognosis and related mechanisms of gastric cancer by targeting miR-129-5p","authors":"Zhenhua Wang, Zhengliang Li, Xiaojing Liu, Jundong Wang, Jiaxi Wang, Guoxiang Jiang, Haizhou Yu","doi":"10.1615/jenvironpatholtoxicoloncol.2024053208","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053208","url":null,"abstract":"Gastric cancer, a prevalent malady within the digestive tract, has a complex pathological mechanism and numerous patients. The regulation of gastric cancer process by long non-coding RNA (lncRNA) has laid a new exploration idea for the study of its molecular mechanism and the treatment of patients. The abnormal expressed genes in gastric cancer were screened by GSE193109 dataset. The correlation between LINC01278 and the likelihood of survival in patients suffering from gastric cancer was investigated by Kaplan-Meier survival curve and multivariate Cox analysis. LINC01278 in gastric cancer tissue samples and cells was verified via RT-qPCR. The CCK-8 and Transwell assay were selected to detect the growth activity of gastric cancer cells. The association between LINC01278 and miR-129-5p was validated through luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay. Correlation analysis of clinical features revealed an association between LINC01278 and the prognosis in gastric cancer patients. LINC01278 was actively expressed in gastric cancer, which exerts a tumor-promoting effect. Silencing LINC01278 suppressed the biological function of tumor cells through spongiform miR-129-5p. LINC01278 has the potential to serve as a novel biomarker, offering new avenues of research for the prognosis and treatment of gastric cancer.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"27 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140560368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024052948
Ye Cheng, Ping Wang, Lidan Liu
Ovarian cancer is one of the most common malignant tumors in female reproductive organs. Its incidence rate is second only to uterine body cancer and cervical cancer, posing a serious threat to women's health. Herein, we explored that PFKFB3 in cancer progression of Ovarian cancer and its underlying mechanism. All the serum samples from Ovarian cancer were collected by our hospital. PFKFB3 mRNA expressions in patients with Ovarian cancer and Ovarian cancer cell lines were up-regulated. PFKFB3 protein expressions in Ovarian cancer cells were induced. Ovarian cancer patients with high PFKFB3 expression had lower survival rate. PFKFB3 gene promoted cell proliferation and EDU cells, and increased cell metastasis of Ovarian cancer. Si-PFKFB3 reduced cell proliferation and EDU cells, and decreased cell metastasis of Ovarian cancer. PFKFB3 gene up-regulation reduced caspase-3/9 activity levels of Ovarian cancer. Si-PFKFB3 also promoted caspase-3/9 activity levels of Ovarian cancer. PFKFB3 gene promoted Warburg effect progression of Ovarian cancer. PFKFB3 gene reduced NLRP3-induced pyroptosis of Ovarian cancer. PFKFB3 suppressed NLRP3 expression. NLRP3 was one target spot for PFKFB3 on pyroptosis of Ovarian cancer. Taken together, we conclude that PFKFB3 suppressed NLRP3 axis to reduce pyroptosis and increase Warburg effect progression of Ovarian cancer, and provide molecular insight into the mechanisms by which the PFKFB3 regulates pyroptosis of Ovarian cancer.
{"title":"PFKFB3 regulated the growth and migration of ovarian cancer cells","authors":"Ye Cheng, Ping Wang, Lidan Liu","doi":"10.1615/jenvironpatholtoxicoloncol.2024052948","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024052948","url":null,"abstract":"Ovarian cancer is one of the most common malignant tumors in female reproductive organs. Its incidence rate is second only to uterine body cancer and cervical cancer, posing a serious threat to women's health. Herein, we explored that PFKFB3 in cancer progression of Ovarian cancer and its underlying mechanism. All the serum samples from Ovarian cancer were collected by our hospital.\u0000PFKFB3 mRNA expressions in patients with Ovarian cancer and Ovarian cancer cell lines were up-regulated. PFKFB3 protein expressions in Ovarian cancer cells were induced. Ovarian cancer patients with high PFKFB3 expression had lower survival rate. PFKFB3 gene promoted cell proliferation and EDU cells, and increased cell metastasis of Ovarian cancer. Si-PFKFB3 reduced cell proliferation and EDU cells, and decreased cell metastasis of Ovarian cancer. PFKFB3 gene up-regulation reduced caspase-3/9 activity levels of Ovarian cancer. Si-PFKFB3 also promoted caspase-3/9 activity levels of Ovarian cancer. PFKFB3 gene promoted Warburg effect progression of Ovarian cancer. PFKFB3 gene reduced NLRP3-induced pyroptosis of Ovarian cancer. PFKFB3 suppressed NLRP3 expression. NLRP3 was one target spot for PFKFB3 on pyroptosis of Ovarian cancer.\u0000Taken together, we conclude that PFKFB3 suppressed NLRP3 axis to reduce pyroptosis and increase Warburg effect progression of Ovarian cancer, and provide molecular insight into the mechanisms by which the PFKFB3 regulates pyroptosis of Ovarian cancer.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"85 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140627926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: The incidence of breast cancer, a malignant tumor that causes more harm to women, is increasing year by year, affecting women at a younger age. This paper describes the possible practical significance of EBLN3P in predicting the prognosis of invasive breast cancer. Methods: EBLN3P and miR-144-3p levels in tissues and cells were detected by real-time quantitative PCR (RT-qPCR). The association between EBLN3P expression and prognosis of invasive breast cancer was investigated using Cox multivariate regression and Kaplan-Meier curve. The growth efficacy of EBLN3P expression on invasive breast cancer cells was evaluated by Cell Counting kit-8 (CCK-8) method and Transwell method, and the mechanism of EBLN3P targeting miR-144-3p was further studied. Results: EBLN3P was elevated in invasive breast cancer, whereas survival rates were lower in patients with high EBLN3P level. EBLN3P directly targeted miR-144-3p to participate in the mechanism of invasive breast cancer, and EBLN3P knockdown had an inhibitory effect on tumor cells. Conclusion: Silencing EBLN3P inhibited the advancement of invasive breast cancer and was expected to be a promising therapeutic target for clinical intervention and prognosis.
{"title":"Silencing the lncRNA EBLN3P alleviates poor prognosis in patients with invasive breast cancer by directly targeting miR-144-3p","authors":"Miao Hu, Min Zhang, Xunjing Qi, Lijuan Yuan, Zhijiao Wu, Yuanyuan Tian, Anning Qi","doi":"10.1615/jenvironpatholtoxicoloncol.2024053299","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053299","url":null,"abstract":"Background: The incidence of breast cancer, a malignant tumor that causes more harm to women, is increasing year by year, affecting women at a younger age. This paper describes the possible practical significance of EBLN3P in predicting the prognosis of invasive breast cancer.\u0000Methods: EBLN3P and miR-144-3p levels in tissues and cells were detected by real-time quantitative PCR (RT-qPCR). The association between EBLN3P expression and prognosis of invasive breast cancer was investigated using Cox multivariate regression and Kaplan-Meier curve. The growth efficacy of EBLN3P expression on invasive breast cancer cells was evaluated by Cell Counting kit-8 (CCK-8) method and Transwell method, and the mechanism of EBLN3P targeting miR-144-3p was further studied.\u0000Results: EBLN3P was elevated in invasive breast cancer, whereas survival rates were lower in patients with high EBLN3P level. EBLN3P directly targeted miR-144-3p to participate in the mechanism of invasive breast cancer, and EBLN3P knockdown had an inhibitory effect on tumor cells.\u0000Conclusion: Silencing EBLN3P inhibited the advancement of invasive breast cancer and was expected to be a promising therapeutic target for clinical intervention and prognosis.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"31 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140800669","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Around 2 million people have been diagnosed with lung carcinoma every year, and 20,000 die from it. Amongst this around 80–85% of lung cancers belong to the category of non-small cell carcinomas. Throughout the last few decades, lung cancer's chromosomal makeup has been better understood, changing clinical care and treatment of advanced or metastatic non-small cell lung cancer patients. This has been possible as a result of high-tech molecular procedures and chromosomal analysis. Due to the discovery of persistent genetic abnormalities, specific drugs have increased lung cancer patients' median survival times. Patients now receive tailored drugs based on genetic abnormalities or other prognostic indicators in pulmonary pathology and oncology. Many testing methods, each with pros and cons, complicate diagnosis algorithms. However, current consensus standards and recommendations have standardized lung cancer diagnostic testing. This article discusses the molecular genetic landscape of the non-small cell lung cancer and the latest therapy developments, focusing on clinically relevant changes.
{"title":"Molecular Pathogenesis, Organ Metastasis, and Targeted Therapy for Non-Small Cell Lung Cancer (NSCLC)","authors":"Salik Abdullah, Ratul Chakraborty, Pratiksha Somnath Kumkar, Biplab Debnath, Asis Bala","doi":"10.1615/jenvironpatholtoxicoloncol.2024051317","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024051317","url":null,"abstract":"Around 2 million people have been diagnosed with lung carcinoma every year, and 20,000 die from it. Amongst this around 80–85% of lung cancers belong to the category of non-small cell carcinomas. Throughout the last few decades, lung cancer's chromosomal makeup has been better understood, changing clinical care and treatment of advanced or metastatic non-small cell lung cancer patients. This has been possible as a result of high-tech molecular procedures and chromosomal analysis. Due to the discovery of persistent genetic abnormalities, specific drugs have increased lung cancer patients' median survival times. Patients now receive tailored drugs based on genetic abnormalities or other prognostic indicators in pulmonary pathology and oncology. Many testing methods, each with pros and cons, complicate diagnosis algorithms. However, current consensus standards and recommendations have standardized lung cancer diagnostic testing. This article discusses the molecular genetic landscape of the non-small cell lung cancer and the latest therapy developments, focusing on clinically relevant changes.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"115 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140036993","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024052122
Ye He, Ya Lin, Chunge Dong, Jie Zhang, Yangli Zhu
Lung adenocarcinoma (LUAD) is a subtype of lung cancer that occurs frequently and results in high mortality and morbidity, comprising almost 50% of all cases with the disease. Previously, long non-coding RNAs (lncRNAs) was evidenced to be helpful in the diagnosis and prognosis of LUAD. lncRNA AGAP11 was identified as a dysregulated lncRNA in LUAD. Whether AGAP11 is linked to the progression and prognosis of LUAD has not been known. The purpose was to probe the action of AGAP11 in the LUAD progression together with its intrinsic mechanism, with a view to supplying a perspective biomarker and therapeutic target for LUAD. AGAP11 expression in LUAD was analyzed by searching in the GEPIA database and conducting RT-qPCR. The significance of AGAP11 for the prognosis of LUAD was assessed by statistical analyses. The targeting relationship between AGAP11 and miR-494-3p was corroborated with Dual-luciferase reporter assay. The role of AGAP11 on cellular processes in LUAD cells was evaluated by CCK-8 and Transwell assays. AGAP11 was markedly down-regulated in LUAD and tightly correlated with TNM stage, lymph node metastasis, and tumor differentiation degree of patients. Down-regulation of AGAP11 was found to predict a dismal prognosis of LUAD. AGAP11 negatively modulated miR-494-3p expression by interacting with it. The growth, migration, and invasion of LUAD cells could be impaired by AGAP11 overexpression, which would be attenuated by the enhanced miR-494-3p expression. AGAP11 acted as a predictor for prognosis and curbed LUAD progression through modulating miR-494-3p.
{"title":"LncRNA AGAP11 suppresses lung adenocarcinoma progression by miR-494-3p and predicts prognosis","authors":"Ye He, Ya Lin, Chunge Dong, Jie Zhang, Yangli Zhu","doi":"10.1615/jenvironpatholtoxicoloncol.2024052122","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024052122","url":null,"abstract":"Lung adenocarcinoma (LUAD) is a subtype of lung cancer that occurs frequently and results in high mortality and morbidity, comprising almost 50% of all cases with the disease. Previously, long non-coding RNAs (lncRNAs) was evidenced to be helpful in the diagnosis and prognosis of LUAD. lncRNA AGAP11 was identified as a dysregulated lncRNA in LUAD. Whether AGAP11 is linked to the progression and prognosis of LUAD has not been known. The purpose was to probe the action of AGAP11 in the LUAD progression together with its intrinsic mechanism, with a view to supplying a perspective biomarker and therapeutic target for LUAD. AGAP11 expression in LUAD was analyzed by searching in the GEPIA database and conducting RT-qPCR. The significance of AGAP11 for the prognosis of LUAD was assessed by statistical analyses. The targeting relationship between AGAP11 and miR-494-3p was corroborated with Dual-luciferase reporter assay. The role of AGAP11 on cellular processes in LUAD cells was evaluated by CCK-8 and Transwell assays. AGAP11 was markedly down-regulated in LUAD and tightly correlated with TNM stage, lymph node metastasis, and tumor differentiation degree of patients. Down-regulation of AGAP11 was found to predict a dismal prognosis of LUAD. AGAP11 negatively modulated miR-494-3p expression by interacting with it. The growth, migration, and invasion of LUAD cells could be impaired by AGAP11 overexpression, which would be attenuated by the enhanced miR-494-3p expression. AGAP11 acted as a predictor for prognosis and curbed LUAD progression through modulating miR-494-3p.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"10 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140205403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01DOI: 10.1615/jenvironpatholtoxicoloncol.2024053018
Bingwei Dong
The early diagnostic methods for Non-small cell lung cancer (NSCLC) are limited, lacking effective biomarkers, and the late stage surgery is difficult and has a high recurrence rate. This experiment want to know whether the effects of FBXO45 in arcinogenesis and metastasis of NSCLC. The up-regulation of FBXO45 expression in patients with NSCLC or cell lines were observed. FBXO45 gene promoted metastasis and Warburg effect, and reduced Ferroptosis of NSCLC. FBXO45 induced ZEB1 expression to promote Warburg effect and reduced Ferroptosis of NSCLC. Sh-FBXO45 reduced cancer growth of NSCLC in mice model. FBXO45 decreased the ubiquitination of ZEB1, leading to increased expression of ZEB1, which in turn promoted the Warburg effect and reduced Ferroptosis in NSCLC. In vivo imaging, Sh-FBXO45 also reduced ZEB1 expression levels of lung tissue in mice model. FBXO45 in NSCLC through activating the Warburg effect, and the inhibition of Ferroptosis of NSCLC by the suppression of ZEB1 ubiquitin, FBXO45 may be a potential therapeutic strategy for NSCLC.
{"title":"FBXO45 expression levels Correlation with cancer severity by ZEB1 ubiquitin in non-small cell lung cancer","authors":"Bingwei Dong","doi":"10.1615/jenvironpatholtoxicoloncol.2024053018","DOIUrl":"https://doi.org/10.1615/jenvironpatholtoxicoloncol.2024053018","url":null,"abstract":"The early diagnostic methods for Non-small cell lung cancer (NSCLC) are limited, lacking effective biomarkers, and the late stage surgery is difficult and has a high recurrence rate. This experiment want to know whether the effects of FBXO45 in arcinogenesis and metastasis of NSCLC.\u0000The up-regulation of FBXO45 expression in patients with NSCLC or cell lines were observed. FBXO45 gene promoted metastasis and Warburg effect, and reduced Ferroptosis of NSCLC. FBXO45 induced ZEB1 expression to promote Warburg effect and reduced Ferroptosis of NSCLC. Sh-FBXO45 reduced cancer growth of NSCLC in mice model. FBXO45 decreased the ubiquitination of ZEB1, leading to increased expression of ZEB1, which in turn promoted the Warburg effect and reduced Ferroptosis in NSCLC. In vivo imaging, Sh-FBXO45 also reduced ZEB1 expression levels of lung tissue in mice model.\u0000FBXO45 in NSCLC through activating the Warburg effect, and the inhibition of Ferroptosis of NSCLC by the suppression of ZEB1 ubiquitin, FBXO45 may be a potential therapeutic strategy for NSCLC.","PeriodicalId":50201,"journal":{"name":"Journal of Environmental Pathology Toxicology and Oncology","volume":"162 1","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140201835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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