MiR-106a targets Mcl-1 to suppress cisplatin resistance of ovarian cancer A2780 cells

Rao, Yumei; Shi, Huirong; Ji, Mei; Chen, Caihong

doi:10.1007/s11596-013-1160-5

Cited by 46 publications

(23 citation statements)

References 28 publications

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“…In the present study, we identified the deregulation of miR-106a in ovarian cancer. miR-106a is widely expressed in diverse human tumors, including gastric, non-small cell lung, pancreatic, colorectal and ovarian cancer (6,8,9,(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53). Previous studies showed that miR-106a acts as a tumor suppressor or an oncogene in different cancers, depending on the different cellular context.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

et al. 2016

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Abstract. Ovarian cancer is a leading cause of malignant gynecological tumor-related mortality among women. The treatment of ovarian cancer patients continues to be challenging. MicroRNA-106a (miR-106a) is widely expressed in diverse human tumors. In the present study, we investigated the biological and pathological roles of miR-106a in ovarian cancers. We found that miR-106a expression was significantly increased in primary ovarian cancer tissues and ovarian cancer cells compared with the level in normal tissues. Ectopic expression of an miR-106a inhibitor attenuated ovarian cancer cell proliferation and invasion. miR-106a promoted the growth and invasion of SKOV3 cells by targeting phosphatase and tensin homolog (PTEN). Furthermore, the present study revealed that IL-6 inhibited miR-106a expression by activating STAT3. Tocilizumab, a humanized anti-human IL-6R antibody, that competitively inhibits IL-6/IL-6R signaling, did not inhibit the proliferation and invasion of SKOV3 cells. In conclusion, our studies revealed that miR-106a was significantly increased in the ovarian cancer tissues and cell lines. Downregulation of the expression of miR-106a inhibited cell growth and metastasis of ovarian cancer cells. Together, the present study suggests that miR-106a acts as an oncogene in ovarian cancers.

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Section: Discussionmentioning

confidence: 99%

“…In non-small cell lung cancers, miR-106a inhibited the growth and metastasis of NSCLC cells by decreasing phosphatase and tensin homolog (PTEN) expression (9). In ovarian cancer, upregulation of miR-106a was found to be associated with paclitaxel and cisplatin resistance (47,50).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

et al. 2016

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“…In ovarian cancer (OV), miR-106a inhibited cell survival and cisplatin resistance, through downregulation of MCL1 (185); conversely expression of miR-106a was higher in cisplatin-resistant OV. miR-106a may be involved in the modulation of cisplatin-induced apoptosis by regulating PDCD4 (186).…”

Section: A Network Analysis: the Most Central Ncrnas In Chemoresistancementioning

confidence: 99%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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Non-coding RNAs (ncRNAs) have been implicated in most cellular functions. The disruption of their function through somatic mutations, genomic imprinting, transcriptional and post-transcriptional regulation, plays an ever-increasing role in cancer development. ncRNAs, including notorious microRNAs, have been thus proposed to function as tumor suppressors or oncogenes, often in a context-dependent fashion. In parallel, ncRNAs with altered expression in cancer have been reported to exert a key role in determining drug sensitivity or restoring drug responsiveness in resistant cells. Acquisition of resistance to anti-cancer drugs is a major hindrance to effective chemotherapy and is one of the most important causes of relapse and mortality in cancer patients. For these reasons, non-coding RNAs have become recent focuses as prognostic agents and modifiers of chemo-sensitivity. This review starts with a brief outline of the role of most studied non-coding RNAs in cancer and then highlights the modulation of cancer drug resistance via known ncRNAs based mechanisms. We identified from literature 388 ncRNA-drugs interactions and analyzed them using an unsupervised approach. Essentially, we performed a network analysis of the non-coding RNAs with direct relations with cancer drugs. Within such a machine-learning framework we detected the most representative ncRNAs-drug associations and groups. We finally discussed the higher integration of the drug-ncRNA clusters with the goal of disentangling effectors from downstream effects and further clarify the involvement of ncRNAs in the cellular mechanisms underlying resistance to cancer treatments.

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“…In this study, miR‐193a was identified as an OVC suppressor as it was found significantly suppressed the proliferation and viability of OVC cell line A2780. Then in 2013, Rao et al found that miR‐106a inhibited OVC cell A2780's survival by suppressing MCL1 gene expression. Then there were miR‐29b, miR‐491‐5p, miR‐509‐3p,, and miR‐142‐5p that were subsequently reported to play proto‐oncogenic or anti‐oncogenic roles in OVC initiation and progression .…”

Section: Discussionmentioning

confidence: 99%

miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene

Cui

Zhang

Zhao

et al. 2019

J of Cellular Biochemistry

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The study of either miR‐153‐3p or MCL1 gene in ovarian carcinoma (OVC) has been reported; however, the interaction between miR‐153‐3p and MCL1 gene in OVC as well as the influence of their interaction on OVC progression has not been reported yet. Herein we intended to study the effects of miR‐153‐3p/MCL1 axis in OVC. Web‐based bioinformatics algorithms including DIANA TarBase 8.0, PicTar, and TargetScan Human 7.2 were used to predict the microRNAs (miRNAs) that could target MCL1 mRNA. Patient characteristics data collection and tissue sample immunohistochemical staining were used to determine the expression level of miR‐153‐3p and MCL1. We determined to unravel the effects of the pairing‐up of miR‐153‐3p and MCL1 mRNA in OVC cell lines (OVCAR3 cell line and A2780) and xenografts (immunodeficient(immunodeficient Rag−/− mice) using several methods including real‐time quantitative reverse transcription polymerase chain reaction, westernWestern blot, colony formation assay, wound healing assay, Transwell invasion assay, flow cytometry assay, and xenograft assay. These experiments were performed to study OVC cellular activities such as cell growth and death and so forth in vitro and in vivo. Plenty of miRNAs that can target MCL1 mRNA have been identified, and we have narrowed them down to miR‐153‐3p. MCL1 gene was found overexpressed in OVC tissues and OVC cell lines at RNA and protein levels, whereas miR‐153‐3p was found under‐expressed in OVC tissues and cells. miR‐153‐3p was found to target MCL1 mRNA and interfered OVC progression. The repression of MCL1 gene expression caused by either miR‐153‐3p or small interfering RNA technique led to significantly reduced OVC cell growth and invasion in vitro. Lastly, the engraftment of transfected human OVC cells into Rag−/− mice confirmed the in vitro results. MCL1 gene acts as a cancer facilitator in OVC. In this study, we revealed the role of miR‐153‐3p on OVC progression by targeting MCL1 gene. Our work could comprehend the current understanding of OVC progression and contribute to the underlying aggression mechanism of this cancer.

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MiR-106a targets Mcl-1 to suppress cisplatin resistance of ovarian cancer A2780 cells

Cited by 46 publications

References 28 publications

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

MicroRNA-106a regulates phosphatase and tensin homologue expression and promotes the proliferation and invasion of ovarian cancer cells

The Network of Non-coding RNAs in Cancer Drug Resistance

miR‐153‐3p regulates progression of ovarian carcinoma in vitro and in vivo by targeting MCL1 gene

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