TES inhibits colorectal cancer progression through activation of p38

Huili Li1, Kun Huang2, Lu Gao3

  • 1Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Oncotarget
|June 22, 2016
PubMed

Insights

The TESTIN (TES) gene suppresses colorectal cancer (CRC) progression by activating p38-MAPK pathways. Reduced TES levels promote CRC, suggesting TES as a potential therapeutic target for colon cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The TESTIN (TES) gene is a candidate tumor suppressor located at a common fragile site.
  • Loss of heterozygosity at this site is observed in various tumors, prompting investigation into its role in colorectal cancer (CRC).

Purpose of the Study:

  • To investigate the role of the TESTIN (TES) gene in colorectal cancer (CRC) progression.
  • To determine the effect of TES protein levels on CRC cell behavior and signaling pathways.

Main Methods:

  • Examined TES protein levels in CRC tissues and cell lines.
  • Utilized gene overexpression and shRNA-mediated knockdown to assess TES function in colon cancer cells.
  • Analyzed the impact of TES on apoptosis, proliferation, migration, invasion, and p38 MAPK signaling.

Main Results:

  • TES protein levels were significantly reduced in CRC tissues and cell lines.
  • Overexpression of TES inhibited CRC cell proliferation, migration, and invasion, while promoting apoptosis.
  • TES knockdown produced opposite effects, increasing CRC progression.
  • TES functions by up-regulating pro-apoptotic proteins, down-regulating anti-apoptotic proteins, and activating p38 MAPK signaling.

Conclusions:

  • TESTIN (TES) acts as a crucial suppressor of colorectal cancer progression.
  • TES exerts its tumor-suppressive function through the activation of p38-MAPK signaling pathways.
  • TES holds potential for CRC diagnosis and targeted gene therapy.

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