Micro-RNAs associated with the evolution of ovarian cancer cisplatin resistance

Boac, Bernadette M.; Xiong, Yin; Marchion, Douglas C.; Abbasi, Forough; Bush, Stephen H.; Ramírez, Ingrid; Khulpateea, B.R.; McClung, C Robertson; Berry, Amy; Zgheib, Nadim Bou; Chon, Hye Sook; Shahzad, Mian M.K.; Judson, Patricia L.; Apte, Sachin M.; Berglund, Anders; Magliocco, Anthony M.; Lancaster, Johnathan M.

doi:10.1016/j.ygyno.2015.12.026

Cited by 17 publications

(12 citation statements)

References 39 publications

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“…These data suggest that miR-31-5p can mediate OXA resistance. Previous studies informed us that miRNAs can mediate cellular sequestration through the mediation of multidrug-resistant proteins and the alteration of calcium signaling [ 32 – 34 ]. In this study, further fractionation of cellular components revealed a change in lysosomal accumulation, which promoted the expression of possible drug transporters that were bound to lysosomes.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-31-5p regulates chemosensitivity by preventing the nuclear location of PARP1 in hepatocellular carcinoma

Que

Zhou

You

et al. 2018

J Exp Clin Cancer Res

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BackgroundMicroRNAs (miRNAs) posttranscriptionally regulate gene expression and thereby contribute to the modulation of numerous complex and disease-relevant cellular processes, including cell proliferation, cell motility, apoptosis and stress response. miRNA-31-5p is encoded on a genomic fragile site, 9p21.3, which is reportedly lost in many hepatocellular carcinoma (HCC) tumors. Based on previous findings, we hypothesized that miR-31-5p alters chemosensitivity and that miR-31-5p mimics may influence sensitivity to chemotherapeutics in HCC as well as in a variety of other cancers.MethodsMiR-31-5p and PARP1 in HCC tissues were tested by RT-PCR and histological analysis, respectively. Next, clonogenic assay and western blot were used to detect miR-31-5p and PARP1 to modulate sensitivity to OXA-based chemotherapy. The distribution of OXA in the nuclear and intracellular was detected by ICP-MS. Coimmunoprecipitation was used to characterize the protein-protein interaction between PARP1 and ABCB9. A xenograft nude mouse model was used to examine the in vivo effects of miR-31-5p.ResultsReintroduction of miR-31-5p into miR-31-5p-null Hep3B cells significantly enhanced clonogenic resistance to oxaliplatin. Although miR-31-5p re-expression increased chemoresistance, it paradoxically increased the relative intracellular accumulation of oxaliplatin. This effect was coupled with a significantly decreased intranuclear concentration of oxaliplatin by ICP-MS. miR-31-5p prevents the nuclear location of PARP1 detected by immunofluorescence, histological analysis and Western blotting analysis. We subsequently identified an indirect miR-31-5p-mediated upregulation of ABCB9, which is a transporter associated with drug accumulation in lysosomes, along with an increased uptake of oxaliplatin to lysosomes; these phenomena were associated with a downregulation of PARP1, a bipotential transcriptional regulator with multiple miR-31-5p binding sites. However, the indirect overexpression of ABCB9 promoted cellular chemosensitivity, suggesting that miR-31-5p promotes chemoresistance largely via an ABCB9-independent mechanism.ConclusionsOverall, our data suggest that the loss of miR-31-5p from HCC tumors promotes chemosensitivity, and this knowledge may be prognostically beneficial in the context of therapeutic sensitivity.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0930-0) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-31-5p regulates chemosensitivity by preventing the nuclear location of PARP1 in hepatocellular carcinoma

Que

Zhou

You

et al. 2018

J Exp Clin Cancer Res

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“…miR-9 inhibits the proliferation, migration, and invasion of serous OVCa cells by blocking TLN1-mediated FAK/AKT pathway [ 44 ]. In addition, expression of miR-496, miR-152, miR-422b, and miR17-3p correlates with acquired cisplatin resistance [ 45 ]. The current study demonstrates that miR-551b is over 100-fold higher in the SP cells than in the non-SP population of cells, implicating that this microRNA is required to maintain the phenotypic features of the SP cells.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Foxo3 and TRIM31 by miR-551b in side population promotes cell proliferation, invasion, and drug resistance of ovarian cancer

et al. 2016

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Ovarian cancer (OVCa) stem cells are associated with tumor growth, metastasis, and recurrence, which are driving forces behind a majority of the OVCa-related mortality. This subpopulation of cancer cells are characterized by uncontrolled proliferation, high invasiveness, and resistance against the current platinum-based therapy. Thus, targeting OVCa cancer stem cells has been focused in recent therapeutic development. Isolation and purification of cancer stem cells are, however, challenging for the lack of sensitive and specific markers. In this study, we demonstrated that miR-551b was upregulated in OVCa stem cells, by using a quantitative PCR array, correlating with the pathological grades of this malignancy. In vitro experiments indicated that miR-551b promoted the proliferation, invasion, and chemoresistance of OVCa cells and cancer stem cells. Further analysis suggested that miR-551b functioned through the suppression of Foxo3 and TRIM31, two important tumor suppressors. In support of this, our in vivo experiments using mouse xenograft models showed that inhibiting miR-551b significantly increased the susceptibility of OVCa cells to cisplatin and prolonged the survival of the host mice. In conclusion, our study suggested miR-551b as a potential biomarker for OVCa stem cells and explored its functional mechanism, providing a potential therapeutic target for future drug development.Electronic supplementary materialThe online version of this article (doi:10.1007/s12032-016-0842-9) contains supplementary material, which is available to authorized users.

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“…Cisplatin (DDP) is a cell cycle non-specific antineoplastic drug, which is applicable for the treatment of several types of cancers and it is also recommended to applied to chemotherapy for epithelial malignancies, such as lung cancer [ 14 ], ovarian cancer [ 15 ], testicular cancer [ 16 ] and cervical cancer [ 17 ]. DDP and its derivatives have been found to have encouraging anti-cancer effects on different types of cancers [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Synergism of ursolic acid and cisplatin promotes apoptosis and enhances growth inhibition of cervical cancer cells via suppressing NF-κB p65

Hou

et al. 2017

Oncotarget

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ObjectiveThis study was designed to investigate the effect of combination of ursolic acid (UA) with cisplatin (DDP) on cervical cancer cell proliferation and apoptosis.MethodsThe mRNA and protein expressions of nuclear factor-kappa B (NF-κB) p65 in cervical cancer cells were examined using RT-PCR and western blot. MTT and colony formation assays were performed to examine the DDP toxicity and the proliferation ability of cervical cancer cells. Cell morphology was observed by means of Hoechst33258 and transmission electron microscopy (TEM). The apoptosis rate and cell cycle were assessed through flow cytometry assay. Western blot was used to detect the expression of apoptosis-related molecules.ResultsThe mRNA and protein expressions of NF-κB p65 in cervical cancer cells were significantly higher than that in cervical epithelial cells. The combined treatment of UA and DDP inhibited cervical cancer cell growth and promoted apoptosis more effectively than DDP treatment or UA treatment alone (P < 0.05). Compared with the DDP group and UA group, the expressions of Bcl-2 and NF-κB p65 in DDP +UA group were decreased, while the expressions of Bax, Caspase-3 and PARP cleavage were observably increased. The expression of nuclear NF-κB p65 significantly reduced in UA group and DDP +UA group. si-p65 group displayed a decrease of cell proliferation ability and led to a significant reduction in the number of SiHa cell colony formation.ConclusionThe combination of UA with DDP could more effectively inhibit SiHa cells proliferation and facilitate cell apoptosis through suppressing NF-κB p65.

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Micro-RNAs associated with the evolution of ovarian cancer cisplatin resistance

Cited by 17 publications

References 39 publications

RETRACTED ARTICLE: MicroRNA-31-5p regulates chemosensitivity by preventing the nuclear location of PARP1 in hepatocellular carcinoma

RETRACTED ARTICLE: MicroRNA-31-5p regulates chemosensitivity by preventing the nuclear location of PARP1 in hepatocellular carcinoma

Downregulation of Foxo3 and TRIM31 by miR-551b in side population promotes cell proliferation, invasion, and drug resistance of ovarian cancer

Synergism of ursolic acid and cisplatin promotes apoptosis and enhances growth inhibition of cervical cancer cells via suppressing NF-κB p65

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