Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MicroRNAs (miRs) have been recently shown to be heavily involved in the development of alcoholic liver disease (ALD) and suggested as a potential therapeutic target in ALD. The miR-34a was consistently reported to be significantly elevated in several ALD rodent models, but it remains unclear how miR-34a modulates the cellular behaviours of hepatocytes in ALD development and progression. This study aims to characterize alcohol-induced miR-34a impact on hepatocytes growth and apoptosis. The miRNA array was performed to assess changes in miRNA after chronic alcohol feeding. Liver and blood samples were used to examine ALD progression. The miR-34a was overexpressed in human hepatocytes to evaluate its impact on cell growth and apoptosis. Real-time quantitative PCR and Western blot were used to determine the growth and apoptosis molecular signalling pathways associated with miR-34a. Alcohol feeding significantly promoted fatty liver progression, serum ALT levels, apoptosis and miR-34a expression in rat liver. Overexpression of miR-34a in human hepatocytes suppressed cell growth signallings, including c-Met, cyclin D1 and cyclin-dependent kinase 6 (CDK6). The miR-34a might also inhibit the expression of sirtuin 1 (Sirt1) and its target, B-cell lymphoma 2. Interestingly, the expression of miR-34a reverses the suppressive effects of ethanol on cell growth. But, miR-34a promotes hepatocyte senescence and apoptosis. Although the miR-34a-mediated down-regulation of cell growth-associated genes may contribute to cell growth retardation, other miR-34a targets, such as Sirt1, may reverse this phenotype. Future studies will be needed to clarify the role of miR-34a in ALD progression.
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PMID:Alcohol-mediated miR-34a modulates hepatocyte growth and apoptosis. 2987 78

Lung cancer is the most common cause of cancer death, approximately 85% of which are non-small cell lung cancer (NSCLC). Here we found that artemether (ART), a natural derivative of artemisinin, significantly inhibits the proliferation of NSCLC cells in a dose- and time-dependent manner. We also demonstrated that high concentration of ART induces apoptosis in NSCLC cells through down-regulating the level of anti-apoptotic protein B-cell lymphoma-2 (Bcl-2), cellular inhibitor of apoptosis protein 1 (cIAP1) and cellular inhibitor of apoptosis protein 2 (cIAP2). While low concentration of ART inhibits the mRNA level of cell cycle related genes including cyclin-dependent kinase 1 (CDK1), cyclin-dependent kinase 2 (CDK2), cyclin-dependent kinase 6 (CDK6), cyclin A2, cyclin B1 and cyclin D1, leading to cell cycle arrest in NSCLC cells. Moreover, we confirmed that low concentration of ART induces DNA double-stranded breaks (DSBs), as well as promoting cellular senescence in NSCLC cells by up-regulating the mRNA and protein level of p16. Taken together, ART represents a promising new anti-NSCLC drug candidate that could attenuate progression of NSCLC cells in a p53-independent manner through inducing apoptosis, cell cycle arrest and promoting cellular senescence.
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PMID:Artemether Attenuates the Progression of Non-small Cell Lung Cancer by Inducing Apoptosis, Cell Cycle Arrest and Promoting Cellular Senescence. 3137 47

Cervical cancer is widely known as one of the most common types of cancer diagnosed in women, and microRNAs (miRNAs) has been characterized as an important regulator in tumor progression, such as cervical cancer. MiR-636 was found to play a tumor suppressor role in hepatocellular carcinoma tumorigenesis. However, the tumorigenic mechanism of miR-636 on cervical cancer has not yet been found. In the present study, we first found that miR-636 was significantly downregulated in cervical cancer tissues and cell lines. in vitro gain- and loss-of-function assays revealed that overexpression of miR-636 inhibited cell proliferation and induced cell apoptosis, while knockdown of miR-636 reversed the effect on cervical tumorigenesis. Furthermore, cyclin-dependent kinase 6 (CDK6) and B-cell lymphoma 2 (Bcl-2) were characterized as targets of miR-636. Notably, overexpression of CDK6 or Bcl-2 could reverse the inhibitory effect of miR-636 on cervical cancer progression. Mechanistically, miR-636 repressed cell survival by targeting CDK6/Bcl-2 in cervical cancer, which may be the underlying mechanism of miR-636-inhibited cervical progression. In conclusion, our findings clarified the biologic significance of miR-636/CDK6/Bcl-2 axis in cervical cancer progression and suggested the potential therapeutic target ability of miR-636 in treatment of cervical cancer.
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PMID:miR-636 represses cell survival by targeting CDK6/Bcl-2 in cervical cancer. 3188 28