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Genome‐wide transcriptional profiling analysis of all trans retinoic acid‐treated tongue carcinoma SCC‐9 cells
Author(s) -
Dai Yaohui,
Wang Juan,
Xia Juan,
Hong Yun,
Chen Na,
Cheng Bin
Publication year - 2011
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21998
Subject(s) - downregulation and upregulation , retinoic acid , cancer research , gene expression profiling , medicine , microarray analysis techniques , cancer cell , tretinoin , microbiology and biotechnology , cancer , gene expression , biology , gene , biochemistry
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. J. Surg. Oncol. 2011; 104:830–835. © 2011 Wiley Periodicals, Inc.