title: RNA interference targeting CHFR enhances taxol chemosensitivity in endometrial             cancer cells.
abstract: In recent years, it has been reported that CHFR may be a useful biomarker             for chemotherapeutic response to microtubule inhibitors in some tumor cells. The             purpose of the present study was to test the hypothesis and to elucidate the underlying             mechanism in endometrial cancer cells. First, we effectively inhibited CHFR expression             at both the mRNA and protein levels using siRNA targeting the CHFR gene in Ishikawa             and Hec-1a cells. We found that inhibition of CHFR expression significantly enhanced             the cytotoxicity of taxol to both cell types, which was confirmed again by colony             formation assays. Moreover, suppression of CHFR induced a significant increase             of the mitotic index and much lower numbers of cells at the G2/M phase in both             cells treated with taxol, indicating mitotic checkpoint impairment. On the other             hand, the number of apoptotic cells significantly increased in Ishikawa and Hec-1a             cells transfected with CHFR siRNA after treatment with taxol, which was associated             with cyclin B1 nuclear localization. Our data indicate that RNA interference targeting             CHFR can sensitize endometrial cancer cells to taxol and CHFR may be a promising             molecular target to enhance the therapeutic effect of taxol for endometrial cancer.
authors.affiliation: Department of Obstetrics and Gynecology, The Third Affiliated Hospital, Sun Yat-sen University, 510630 Guangzhou, PR China. tigerlee777@163.com
authors.forename: Xiaomao
authors.initials: X
authors.lastname: Li
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Wang
authors.forename: Yuebo
authors.initials: Y
authors.lastname: Yang
authors.forename: Chengfang
authors.initials: C
authors.lastname: Xu
authors.forename: Huimin
authors.initials: H
authors.lastname: Shen
mesh_terms: D021581:Active Transport, Cell Nucleus; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D059447:Cell Cycle Checkpoints; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism; D045744:Cell Line, Tumor; D056744:Cyclin B1 / Q000378:metabolism; D016889:Endometrial Neoplasms; D005260:Female; D015870:Gene Expression; D055785:Gene Knockdown Techniques; D006801:Humans; D008938:Mitosis; D009363:Neoplasm Proteins / Q000235:genetics* / Q000378:metabolism; D017239:Paclitaxel / Q000494:pharmacology*; D000075223:Poly-ADP-Ribose Binding Proteins; D034622:RNA Interference; D044767:Ubiquitin-Protein Ligases
chemical_list: D000972:Antineoplastic Agents, Phytogenic; C534699:CCNB1 protein, human; D018797:Cell Cycle Proteins; D056744:Cyclin B1; D009363:Neoplasm Proteins; D000075223:Poly-ADP-Ribose Binding Proteins; C412002:CHFR protein, human; D044767:Ubiquitin-Protein Ligases; D017239:Paclitaxel