KLF5‑mediated expression of CARD11 promotes the progression of gastric cancer

Qiusen Li1, Sheng Li1, Zongxian Li1

  • 1Department of Gastroenterology, The Second People's Hospital of Wuhu, Wuhu, Anhui 241000, P.R. China.

Insights

Caspase recruitment domain-containing protein 11 (CARD11) drives gastric cancer growth and metastasis. The transcription factor Krüppel-like factor 5 (KLF5) upregulates CARD11, promoting tumor progression and activating the mTOR pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Caspase recruitment domain-containing protein 11 (CARD11) is implicated in various cancers.
  • Its specific role and regulatory mechanisms in gastric cancer remain to be fully elucidated.

Purpose of the Study:

  • To investigate the function and mechanism of CARD11 in gastric cancer.
  • To explore the regulatory relationship between CARD11 and Krüppel-like factor 5 (KLF5).

Main Methods:

  • Analysis of CARD11 expression and patient survival data.
  • In vitro experiments involving CARD11 silencing and KLF5 overexpression in gastric cancer cells.
  • Assessment of cell proliferation, migration, invasion, epithelial-mesenchymal transition (EMT), and signaling pathways (mTOR).

Main Results:

  • High CARD11 expression correlates with poor prognosis in gastric cancer.
  • CARD11 inhibition suppressed proliferation, migration, invasion, and EMT, while inducing cell cycle arrest.
  • KLF5 was identified as a positive regulator of CARD11 transcription.
  • KLF5 overexpression counteracted the effects of CARD11 silencing, promoting proliferation, migration, invasion, and EMT.

Conclusions:

  • CARD11 promotes gastric cancer progression by enhancing proliferation, migration, invasion, and EMT.
  • The KLF5-CARD11 axis plays a critical role in gastric cancer development.
  • CARD11 interference inhibits gastric cancer growth and metastasis, partly through the mTOR pathway.

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