2017
DOI: 10.1007/s00109-017-1539-z
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miR-30a-5p enhances paclitaxel sensitivity in non-small cell lung cancer through targeting BCL-2 expression

Abstract: BCL-2 is a novel direct target of miR-30a-5p. miR-30a-5p enhances NSCLC paclitaxel sensitivity in vitro and in vivo. miR-30a-5p sensitizes NSCLC cells to paclitaxel by inducing apoptosis through BCL-2 inhibition. miR-30a-5p negatively correlates with BCL-2 and predicts a favorable clinical outcome in NSCLC patients.

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Cited by 55 publications
(44 citation statements)
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“…Downregulation of miR-205 confers glioma cells with DDP resistance and pancreatic cancer cells with gemcitabine resistance [21,22]. miR-30a influences chemoresistance in melanoma cells by targeting insulin-like growth factor 1 [23], regulates etoposide/DDP resistance in small cell lung cancer by targeting Beclin-1 [24], sensitizes NSCLC cells to paclitaxel through B-cell lymphoma 2 inhibition [25], and enables acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors to be overcome in NSCLC cells by reducing phosphoinositide-3-kinase regulatory Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry submit 2 [26]. miR-30a decreases multidrug resistance in human gastric cancer cells by modulating cell autophagy [27].…”
Section: Discussionmentioning
confidence: 99%
“…Downregulation of miR-205 confers glioma cells with DDP resistance and pancreatic cancer cells with gemcitabine resistance [21,22]. miR-30a influences chemoresistance in melanoma cells by targeting insulin-like growth factor 1 [23], regulates etoposide/DDP resistance in small cell lung cancer by targeting Beclin-1 [24], sensitizes NSCLC cells to paclitaxel through B-cell lymphoma 2 inhibition [25], and enables acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors to be overcome in NSCLC cells by reducing phosphoinositide-3-kinase regulatory Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry submit 2 [26]. miR-30a decreases multidrug resistance in human gastric cancer cells by modulating cell autophagy [27].…”
Section: Discussionmentioning
confidence: 99%
“…Previous studies have defined miR-30a as a putative tumor suppressor that is frequently dysregulated in cancers including osteosarcoma and cancers of the breast, lung, and head and neck [11,[23][24][25][26][27][28]. One mechanism whereby miR-30 may modulate cancer development is via inhibiting cell proliferation and invasion and by inducing apoptotic cell death [24][25][26][27]. Indeed, miR-30a overexpression is associated with reduced BCL-2 expression in non-small-cell lung cancer, leading to the increased apoptotic death of these cells [24].…”
Section: Biomed Research Internationalmentioning
confidence: 99%
“…CTGF, connective tissue growth factor; GC, gastric cancer; IRF2BP2, interferon regulatory factor 2 binding protein 2; RT-qPCR, real-time quantitative PCR; TEAD4, TEA domain family members 4; VGLL4, vestigial-like family member 4 predicted binding site in the 3′-UTR of IRF2BP2 were identified using TargetScan (http://www.targe tscan.org/) and microRNA.org (http://www.micro rna.org/). Four miRNAs (miR-101-3p, miR-30a-5p, miR-519d-3p and miR-155-5p) reported to play roles in human tumours were chosen [33][34][35][36] ( Figure 6A). The results of Western blotting in the SGC-7901 and BGC-823 cell lines showed that the overexpression of miR-101-3p significantly reduced IRF2BP2 protein expression ( Figure 6B,C); however, the overexpression of miR-101-3p had no significant effect on IRF2BP2 mRNA expression ( Figure 6D).…”
Section: Micror-101-3p Suppresses Ctgf Expression Through Irf2bp2-ymentioning
confidence: 99%