Effects of transforming growth interacting factor on biological behaviors of gastric carcinoma cells
Zhong-Liang Hu1, Ji-Fang Wen, De-Sheng Xiao
1Department of Pathology, Basic Medical Institute, Central South University, Changsha 410078, Hunan Province, China.
Aim:
Transforming growth interacting factor (TGIF) is an inhibitor of both transforming growth factor beta (TGF-beta) and retinoid signaling pathways. Moreover, the activation of MAPK pathway can prolong its half-life. However, its role in carcinogenesis is still unknown. Thus we attempted to investigate the effect of TGIF on biologic behaviors of gastric carcinoma cells.
Methods:
Gastric carcinoma cell line, SGC-7901, was stably transfected with plasmid PcDNA3.1-TGIF. Western blotting and cell immunohistochemistry screening for the highly expressing clone of TGIF were employed. The growth of transfected cells was investigated by MTT and colony-formation assays, and apoptosis was measured by flow cytometry (FCM) and transmission electron microscopy. Tumorigenicity of the transfectant cells was also analyzed.
Results:
TGIF had no effect on the proliferation, cell cycle and apoptosis of SGC-7901 cells, but cellular organelles of cells transfected with TGIF were richer than those of vector control or parental cells. Its clones were smaller than the control ones in plate efficiency, and its tumor tissues also had no obvious necrosis compared with the vector control or parental cells. Moreover, TGIF could resist TGF-beta mediated growth inhibition.
Conclusion:
TGIF may induce differentiation of stomach neoplastic cells. In addition, TGIF can counteract the growth inhibition induced by TGF-beta.
Insights
Transforming growth interacting factor (TGIF) may induce differentiation in stomach cancer cells and counteract growth inhibition by TGF-beta. This study investigated TGIF
Area of Science:
- Molecular biology
- Cancer research
- Cell signaling
Background:
- Transforming growth interacting factor (TGIF) inhibits TGF-beta and retinoid signaling.
- TGIF half-life is prolonged by MAPK pathway activation.
- The role of TGIF in carcinogenesis remains unclear.
Purpose of the Study:
- To investigate the effect of TGIF on the biological behaviors of gastric carcinoma cells.
- To understand TGIF's potential role in stomach cancer development.
Main Methods:
- Stable transfection of SGC-7901 gastric carcinoma cells with TGIF.
- Western blotting and immunohistochemistry for TGIF expression.
- MTT, colony-formation assays, flow cytometry, and electron microscopy to assess cell proliferation, apoptosis, and organelle changes.
- Tumorigenicity analysis.
Main Results:
- TGIF did not affect proliferation, cell cycle, or apoptosis in SGC-7901 cells.
- Transfected cells showed enhanced cellular organelles and reduced clone size.
- TGIF expression resisted TGF-beta-mediated growth inhibition.
- Tumor tissues exhibited less necrosis compared to controls.
Conclusions:
- TGIF may induce differentiation in stomach neoplastic cells.
- TGIF can counteract growth inhibition mediated by TGF-beta.
- TGIF's role in gastric carcinogenesis warrants further investigation.
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