LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer via regulating miR-29c/CDK6 axis

Hualong Zhang1, Bin Zhao1, Xiuxia Wang2

  • 1Department of Breast and Thyroid Surgery, Shanxian Central Hospital, Heze 274300, China.

Life Sciences
|May 4, 2019
PubMed
Abstract

Insights

Long intergenic noncoding RNA 00511 (LINC00511) knockdown boosts paclitaxel efficacy in breast cancer by upregulating miR-29c and downregulating CDK6. This study reveals LINC00511 as a potential therapeutic target for overcoming drug resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Drug resistance is a significant clinical challenge in breast cancer treatment.
  • Long non-coding RNAs (lncRNAs) are implicated in cancer drug resistance.
  • The role of LINC00511 in breast cancer drug resistance is currently unknown.

Purpose of the Study:

  • To investigate the effect of LINC00511 on the drug resistance of breast cancer cells.
  • To elucidate the molecular mechanism underlying LINC00511's role in breast cancer drug resistance.

Main Methods:

  • Gene expression analysis (RT-qPCR) of LINC00511, miR-29c, and CDK6 in breast cancer tissues and cells.
  • Correlation analysis between gene expressions.
  • Luciferase reporter assays, RT-qPCR, and Western blot to explore molecular interactions.
  • MTT assays and flow cytometry to assess paclitaxel cytotoxicity.

Main Results:

  • LINC00511 and CDK6 were upregulated, while miR-29c was downregulated in breast cancer.
  • LINC00511 directly suppressed miR-29c expression, and LINC00511 positively regulated CDK6.
  • Knockdown of LINC00511 enhanced paclitaxel cytotoxicity by upregulating miR-29c.
  • CDK6 was identified as a direct target of miR-29c.

Conclusions:

  • LINC00511 knockdown enhances paclitaxel cytotoxicity in breast cancer cells.
  • The mechanism involves the regulation of the miR-29c/CDK6 axis by LINC00511.
  • LINC00511 is a potential therapeutic target for overcoming paclitaxel resistance in breast cancer.

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