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Genomic-directed targeted therapy increases endometrial cancer cell sensitivity to doxorubicin.

Abstract：

OBJECTIVE:We aimed to utilize genome-wide expression analysis to identify molecular pathways that may contribute to endometrial cancer resistance to doxorubicin (DOX) and that also represent therapeutic targets to increase DOX sensitivity. STUDY DESIGN:Ten endometrial cancer cell lines were subjected to gene expression analysis. Sensitivity of each endometrial cell line to DOX was quantified by dimethylthiazoldiphenyltetrazoliumbromide cell proliferation assay. Pearson's correlation test was used to identify genes associated with response to DOX. Genes associated with DOX responsiveness were analyzed, and identified pathways were subjected to targeted inhibition. RESULTS:Pearson's correlation analysis identified 2871 genes associated with DOX resistance (P < .05), which included members of the Src pathway. Targeted inhibition of the Src pathway increased DOX sensitivity in RL 95-2 (P < .0001), HEC 1B (P < .001), MEF 296 (P < .05), and MEF 280 (P = .14) cell lines. CONCLUSION:Genomic analysis can identify therapeutic targets such as the Src pathway that may influence endometrial cancer DOX sensitivity.

journal_name

Am J Obstet Gynecol

journal_title

American journal of obstetrics and gynecology

authors

Indermaur MD,Xiong Y,Kamath SG,Boren T,Hakam A,Wenham RM,Apte SM,Lancaster JM

doi

10.1016/j.ajog.2010.02.003

subject

Has Abstract

pub_date

2010-08-01 00:00:00

pages

158.e1-40

issue

2

eissn

0002-9378

issn

1097-6868

pii

S0002-9378(10)00208-5

journal_volume

203

pub_type

杂志文章

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