Integrase interactor 1 regulates proliferation, apoptosis and invasion in gastric cancer cells

Xiao-Chun Wang1, Yong Li, Li-Qiao Fan

  • 1Department of General Surgery, the Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, China.

Abstract

Insights

Integrase interactor 1 (INI1) acts as a tumor suppressor in gastric cancer, inhibiting proliferation and invasion while promoting apoptosis. Lower INI1 expression correlates with gastric carcinoma, highlighting its crucial role in cancer development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Integrase interactor 1 (INI1) is a component of the ATP-dependent chromatin remodeling hSWI-SNF complex.
  • INI1 functions as a tumor suppressor in various cancers.
  • The specific role of INI1 in gastric cancer progression remained unclear before this study.

Purpose of the Study:

  • To investigate the effect of INI1 on gastric carcinogenesis.
  • To elucidate the role of INI1 in the progression of gastric cancer.

Main Methods:

  • Analyzed INI1 expression in gastric tumor tissues and adjacent normal tissues using RT-PCR and Western blotting.
  • Overexpressed INI1 in gastric cancer cell line SGC7901 via INI1-GFP transfection.
  • Assessed cell proliferation, cell cycle, apoptosis, migration, and invasion using MTT, FCM, TUNEL, wound healing, and transwell assays.
  • Quantified expression of proliferation, apoptosis, and invasion-related genes.

Main Results:

  • INI1 expression was significantly lower in gastric carcinoma tissues compared to normal tissues.
  • INI1 overexpression in SGC7901 cells suppressed proliferation and invasiveness, increased anoikis, and promoted G(0)/G(1) phase arrest.
  • INI1 upregulation led to increased expression of p16, p21, p53, Bax, and TIMP1, while decreasing cyclin D1, cyclin A, Bcl-2, ICAM1, MMP2, and MMP9.

Conclusions:

  • INI1 plays a critical role in gastric carcinogenesis.
  • INI1 influences gastric cancer progression by modulating cell proliferation, apoptosis, and invasion.

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