Journal of surgical oncology · 2011
Genome-wide transcriptional profiling analysis of all trans retinoic acid-treated tongue carcinoma SCC-9 cells.
Оценочное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Dai Yaohui, Wang Juan, Xia Juan, Hong Yun, Chen Na, Cheng Bin
Аннотация
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.
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.
Предметные рубрики MeSH
Antineoplastic AgentsCase-Control StudiesChemokine CXCL10Dose-Response Relationship, DrugGene Expression ProfilingGene Expression Regulation, NeoplasticGenome-Wide Association StudyHumansIntercellular Adhesion Molecule-1InterleukinsLinear ModelsOligonucleotide Array Sequence AnalysisTongue NeoplasmsTretinoinTumor Cells, Cultured