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TP73-AS1 promotes breast cancer cell proliferation through miR-200a-mediated TFAM inhibition

Jia Yao1, Feng Xu1, Danhua Zhang1

  • 1Department of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, China.

Journal of Cellular Biochemistry
|June 23, 2017
PubMed

Insights

Long non-coding RNA TP73-AS1 is upregulated in breast cancer, promoting tumor growth by sponging miR-200a and increasing TFAM expression. This oncogenic lncRNA may be a therapeutic target for breast cancer.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) play roles in cancer, but TP73-AS1's function in breast cancer (BC) is unclear.
  • TP73-AS1 (PDAM) regulates apoptosis via p53 signaling and is abnormally expressed in cancers.
  • Previous research indicated miR-200a inhibits BC proliferation by targeting TFAM.

Purpose of the Study:

  • To investigate the role and mechanism of TP73-AS1 in breast cancer cell proliferation.
  • To determine the relationship between TP73-AS1 expression and patient prognosis.

Main Methods:

  • Analysis of TP73-AS1 expression in BC tissues and cell lines.
  • In vitro knockdown of TP73-AS1 in BC cell lines.
  • Investigation of TP73-AS1's interaction with miR-200a and TFAM.

Main Results:

  • TP73-AS1 was significantly upregulated in BC tissues and cell lines, correlating with poorer prognosis.
  • Knockdown of TP73-AS1 suppressed BC cell proliferation by regulating TFAM.
  • TP73-AS1 directly targets miR-200a, acting as a competing endogenous RNA (ceRNA) to sponge miR-200a and promote TFAM expression.

Conclusions:

  • TP73-AS1 acts as an oncogenic lncRNA in breast cancer by promoting proliferation.
  • TP73-AS1 functions as a ceRNA for miR-200a, upregulating TFAM.
  • TP73-AS1 represents a potential therapeutic target for breast cancer treatment.
Keywords:
TFAMTP73-AS1breast cancerlncRNAmiR-200a

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