Yaohui Dai1, Juan Wang, Juan Xia, Yun Hong, Na Chen, Bin Cheng. 1. Department of Oral Medicine, Guanghua School of Stomatology and Institute of Stomatological Research, Sun Yat-Sen University, Guangzhou, Guangdong, People's Republic of China.
Abstract
BACKGROUND: All trans retinoic acid (ATRA) is used as standard of care in promyelocytic leukemia. Not much is known about the gene expression profile in ATRA-treated tongue cancer cells. We performed a genome-wide transcriptional profiling of ATRA-treated tongue cancer cells to understand the pathways that mediate ATRA action in tongue cancer. METHODS: We measured the effects of ATRA on the proliferation of SCC-9 human tongue carcinoma cells. The differential gene expression profile was measured by microarray analysis of untreated and ATRA-treated cells and expression of key genes was validated by real-time RT-PCR. RESULTS: ATRA treatment (24 and 48 hr) significantly inhibited SCC-9 cell proliferation in a dose-dependent manner. SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Validation by real-time PCR showed a significant upregulation of intracellular adhesion molecule 1 (ICAM1) and downregulation of CXCL10 and IL32. CONCLUSIONS: ATRA had an anti-tumor effect in tongue cancer cells. This effect is likely mediated via upregulation of ICAM1 and downregulation of CXCL10 and IL32.
BACKGROUND: All trans retinoic acid (ATRA) is used as standard of care in promyelocytic leukemia. Not much is known about the gene expression profile in ATRA-treated tongue cancer cells. We performed a genome-wide transcriptional profiling of ATRA-treated tongue cancer cells to understand the pathways that mediate ATRA action in tongue cancer. METHODS: We measured the effects of ATRA on the proliferation of SCC-9 humantongue carcinoma cells. The differential gene expression profile was measured by microarray analysis of untreated and ATRA-treated cells and expression of key genes was validated by real-time RT-PCR. RESULTS:ATRA treatment (24 and 48 hr) significantly inhibited SCC-9 cell proliferation in a dose-dependent manner. SCC-9 cells treated for 48 hr with ATRA showed upregulation of 276 genes, including ANGPTL4, GDF15, ICAM1 and TUSC4, and downregulation of 43 genes, including CXCL10. Validation by real-time PCR showed a significant upregulation of intracellular adhesion molecule 1 (ICAM1) and downregulation of CXCL10 and IL32. CONCLUSIONS:ATRA had an anti-tumor effect in tongue cancer cells. This effect is likely mediated via upregulation of ICAM1 and downregulation of CXCL10 and IL32.