Chidamide modulates proliferation, migration and apoptosis of human tongue squamous carcinoma SCC9 cells through multiple signaling pathways
Keywords:Chidamide, tongue squamous cell carcinoma, apoptosis, epigenetic modulation, cell migration
- The prognosis of current treatment of tongue squamous cell carcinoma (TSCC) is not optimistic. Development of new pharmacological agents targeting TSCC is a priority.
- The anti-tumor effect of chidamide, a histone deacetylase inhibitor, was examined in vitro in TSCC SCC9 cells using cell viability and wound healing assays, flow cytometry analysis and Western blotting.
- Chidamide inhibited cell viability and migration through ERK, mTOR and E-cadherin It induced apoptosis via the Bcl-2/caspase-3 pathway.
- Chidamide has the potential to be developed into a new therapeutic agent for TSCC treatment.
Abstract: Chidamide, a histone deacetylase (HDAC) inhibitor, displays antitumor activities in different tumor cells. Tongue squamous cell carcinoma (TSCC) is the most prevalent oral cavity malignancy with a high incidence and a high mortality rate. We describe the antitumor effects of chidamide on human TSCC SCC9 cells, which has not been reported before. Cell viability and wound healing assay and flow cytometry analysis were used to determine the proliferation, migration, cell cycle and apoptosis of chidamide-treated SCC9 cells in vitro. Western blotting was used to detect relative changes in protein levels. Our results reveal that chidamide inhibits SCC9 cell proliferation by decreasing ERK1/2 and mTOR phosphorylation and arresting the cell cycle in G0/G1 phase. Chidamide decreased cell migration in dose- and time-dependent manner by increasing E-cadherin expression. Chidamide induced SCC9 cells apoptosis by increasing the level of cleaved caspase-3 and decreasing the expression of Bcl-2. To sum up, chidamide displayed potent antitumor effects on SCC9 cells through multiple signaling pathways and has the potential to be developed as a new therapeutic agent to treat TSCC.
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