MicroRNA-101 inhibits cell progression and increases paclitaxel sensitivity by suppressing MCL-1 expression in human

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Updated: Apr 11, 2026

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
09:45

An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells

Published on: May 21, 2019

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Xiaoping Liu1, Hailin Tang1, Jianping Chen2

  • 1Department of Breast Oncology, Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, Guangdong, China.

Oncotarget
|June 4, 2015
PubMed

Insights

MicroRNA-101 (miR-101) is decreased in aggressive triple-negative breast cancer (TNBC). Restoring miR-101 enhances paclitaxel sensitivity by inhibiting MCL-1, offering potential new TNBC therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with limited treatment options.
  • Understanding molecular mechanisms driving TNBC chemoresistance is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the roles of miR-101 and MCL-1 in paclitaxel sensitivity in TNBC.
  • To explore the therapeutic potential of targeting the miR-101/MCL-1 axis in TNBC.

Main Methods:

  • Analysis of miR-101 and MCL-1 expression in TNBC tissues and cell lines.
  • In vitro and in vivo studies of miR-101 overexpression effects on TNBC.
  • Luciferase assays to confirm MCL-1 as a direct miR-101 target.
  • Assessment of MCL-1 suppression and miR-101 effects on paclitaxel sensitivity.

Main Results:

  • miR-101 expression was significantly decreased in TNBC tissues and cell lines.
  • Overexpression of miR-101 inhibited TNBC cell growth, induced apoptosis, and suppressed tumor formation.
  • MCL-1 was overexpressed in TNBC and confirmed as a direct target of miR-101.
  • miR-101 inhibited MCL-1 expression, and suppression of MCL-1 enhanced paclitaxel sensitivity in TNBC cells.

Conclusions:

  • miR-101 plays a tumor-suppressive role in TNBC by inhibiting MCL-1.
  • The miR-101/MCL-1 pathway is a critical determinant of paclitaxel sensitivity in TNBC.
  • Targeting miR-101 or MCL-1 may represent a novel therapeutic strategy for improving paclitaxel efficacy in TNBC patients.
Keywords:
MCL-1miR-101paclitaxelsensitivitytriple-negative breast cancer

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