Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0026764 (multiple myeloma)
 36,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous studies confirmed that aberrant miRNAs expression contributes to multiple myeloma (MM) development and progression. However, the roles of specific miRNAs in MM remain to be investigated. In present study, we demonstrated that miR-410 expression was increased in MM newly diagnosed and relapsed tissues and cell lines. Clinical analysis revealed that miR-410 was positively correlated with advanced ISS stage. Moreover, high miR-410 expression in MM patients showed an obvious shorter overall survival and progression-free survival. Gain- and loss-of function experiments indicated that miR-410 promoted cell proliferation, cell cycle progression and apoptosis inhibition both in vitro and in vivo. Moreover, KLF10 was identified as a direct downstream target of miR-410 in MM cells, and mediated the functional influence of miR-410 in MM, resulting in PTEN/AKT activation. In clinical samples of MM, miR-410 inversely correlated with KLF10. Alteration of KLF10 expression or AKT inhibitor at least partially abolished the biological effects of miR-410 on MM cells. Furthermore, downregulated expression of lncRNA OIP5-AS1 was inversely correlated with miR-410 expression in MM tissues. LncRNA OIP5-AS1 could modulate the miR-410 expression and regulate its target KLF10/PTEN/AKT-mediated cellular behaviors. Taken together, this research supports the first evidence that lncRNA OIP5-AS1 loss-induced miR-410 accumulation facilitates cell proliferation, cycle progression and apoptosis inhibition by targeting KLF10 via activating PTEN/PI3K/AKT pathway in MM.
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PMID:LncRNA OIP5-AS1 loss-induced microRNA-410 accumulation regulates cell proliferation and apoptosis by targeting KLF10 via activating PTEN/PI3K/AKT pathway in multiple myeloma. 2879 57

Long noncoding RNAs (lncRNAs) have been reported to play a significant role in the occurrence and progression of tumors. In different tumors, they can either act as an oncogene or tumor suppressor via modulating various target mRNAs. OIP5-AS1 belongs to lncRNA family. It has been reported to be involved in the tumorigenesis of some cancers, such as bladder cancer, gastric cancer, and multiple myeloma. However, the role it plays in hepatocellular carcinoma (HCC) remains unclear. This study aims to explore the inherent mechanism of lncRNA OIP5-AS1 in HCC. In the first place, qRT-PCR found that OIP5-AS1 and VEGFA expressions were significantly increased while miR-3163 was obviously reduced in HCC cells and tissues. Next, a series of functional experiments found that knockdown of OIP5-AS1 suppressed HCC cell proliferation, migration and angiogenesis abilities while promoting cell apoptosis simultaneously. Last but not least, miR-3163 inhibition or VEGFA overexpression can reverse the anti-tumor effect of OIP5-AS1. In summary, OIP5-AS1 affects HCC proliferation, metastasis, and angiogenesis in HCC by regulating VEGFA expression through sponging miR-3163.
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PMID:LncRNA OIP5-AS1 promotes cell proliferation and migration and induces angiogenesis via regulating miR-3163/VEGFA in hepatocellular carcinoma. 3232 64