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Overexpression of SASH1 Inhibits TGF-β1-Induced EMT in Gastric Cancer Cells

Wei Zong1, Chen Yu, Ping Wang

  • 1Department of Gastroenterology, Shaanxi Provincial People's Hospital, the Third Affiliated Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an, China.

Oncology Research
|May 15, 2016
PubMed

Insights

SAM and SH3 domain-containing 1 (SASH1) suppresses gastric cancer cell invasion. SASH1 inhibits transforming growth factor (TGF)-β1-induced epithelial-mesenchymal transition (EMT) via the PI3K/Akt pathway, suggesting SASH1 as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Epithelial-mesenchymal transition (EMT) is crucial for gastric cancer metastasis.
  • SAM and SH3 domain-containing 1 (SASH1) is a potential tumor suppressor, but its role in gastric cancer is unclear.

Purpose of the Study:

  • To investigate the effect of SASH1 on gastric cancer cell behavior.
  • To determine SASH1's impact on transforming growth factor (TGF)-β1-induced EMT.

Main Methods:

  • Assessed SASH1 expression in gastric cancer cells.
  • Examined SASH1's effect on TGF-β1-treated gastric cancer cells (TSGH cells).
  • Analyzed cell migration, invasion, and PI3K/Akt signaling pathway activity.

Main Results:

  • SASH1 expression was low in gastric cancer cells and inhibited by TGF-β1.
  • SASH1 suppressed TGF-β1-induced EMT, cell migration, and invasion.
  • SASH1 inhibited PI3K and Akt phosphorylation in TGF-β1-stimulated cells.

Conclusions:

  • SASH1 inhibits TGF-β1-induced EMT in gastric cancer via the PI3K/Akt pathway.
  • SASH1 demonstrates potential as a therapeutic target for gastric cancer treatment.

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