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Long intergenic non-coding RNA APOC1P1-3 inhibits apoptosis by decreasing α-tubulin acetylation in breast cancer

X-H Liao1, J-G Wang2, L-Y Li1

  • 1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, No. 138 Yixueyuan Road, Shanghai, China.

Cell Death & Disease
|May 27, 2016
PubMed

Insights

This study identifies long intergenic non-coding RNA APOC1P1-3 (lincRNA-APOC1P1-3) as overexpressed in breast cancer. Overexpression of lincRNA-APOC1P1-3 inhibits breast cancer cell apoptosis by affecting tubulin acetylation and caspase-3 activity.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Long non-coding RNAs (lncRNAs) are increasingly recognized as crucial regulators in tumor development.
  • The specific functions of lncRNAs in breast cancer pathogenesis are not yet fully understood.

Purpose of the Study:

  • To identify and characterize aberrantly expressed lncRNAs in breast cancer.
  • To elucidate the role and mechanism of lincRNA-APOC1P1-3 in breast cancer progression.

Main Methods:

  • Microarray analysis to identify differentially expressed lncRNAs.
  • Quantitative real-time PCR and pyrosequencing for validation and methylation analysis.
  • In vitro functional assays (plasmid transfection, siRNA silencing) and molecular mechanism studies (RNA pull-down, RNA immunoprecipitation).

Main Results:

  • Identified 224 upregulated and 324 downregulated lncRNAs in breast cancer.
  • lincRNA-APOC1P1-3 was found to be overexpressed in breast cancer tissues, correlating with tumor size and promoter hypomethylation.
  • lincRNA-APOC1P1-3 directly binds to tubulin, reducing α-tubulin acetylation, inactivating caspase-3, and consequently inhibiting apoptosis.

Conclusions:

  • lincRNA-APOC1P1-3 is a significantly overexpressed lncRNA in breast cancer.
  • Overexpression of lincRNA-APOC1P1-3 promotes breast cancer by inhibiting apoptosis through the regulation of tubulin acetylation and caspase-3 activity.

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