Abstract:
:Acquisition of resistance to paclitaxel is a major obstacle to successful treatment of breast cancer patients, but the molecular mechanisms underlying the development of drug resistance remain largely unclear. The aim of the present study was to investigate the role and mechanism of action of miR‑200c‑3p in the resistance of breast cancer to paclitaxel. It was observed that miR‑200c‑3p expression, as determined by reverse transcription‑quantitative polymerase chain reaction analysis, was significantly downregulated in paclitaxel‑resistant MCF‑7/Tax cells compared with parental MCF‑7 cells. Overexpression of miR‑200c‑3p increased the chemosensitivity to paclitaxel and enhanced apoptosis in MCF‑7/Tax cells, whereas the downregulation of miR‑200c‑3p exerted the opposite effect. In addition, upregulation of miR‑200c‑3p in MCF‑7/Tax cells suppressed the expression of sex‑determining region Y‑box 2 (SOX2) at the mRNA and protein levels. Dual‑luciferase reporter assay demonstrated that SOX2 is a target of miR‑200c‑3p in MCF‑7/Tax cells. Moreover, knockdown of SOX2 expression increased chemosensitivity to paclitaxel and upregulated miR‑200c‑3p expression in MCF‑7/Tax cells. Taken together, the results of the present study indicated that miR‑200c‑3p plays a key role in the development of paclitaxel resistance in breast cancer, possibly partially through regulating SOX2 expression, suggesting that the miR‑200c‑3p‑SOX2 loop may serve as a potential target for the reversal of paclitaxel resistance in breast cancer.
journal_name
Oncol Repjournal_title
Oncology reportsauthors
Chen J,Tian W,He H,Chen F,Huang J,Wang X,Chen Zdoi
10.3892/or.2018.6735subject
Has Abstractpub_date
2018-12-01 00:00:00pages
3821-3829issue
6eissn
1021-335Xissn
1791-2431journal_volume
40pub_type
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