Báo cáo y học: "Functional characterization of Trip10 in cancer cell growth and survival"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Functional characterization of Trip10 in cancer cell growth and survival | Hsu et al. Journal of Biomedical Science 2011 18 12 http content 18 1 12 The cost of publication in Journal of Biomedical Science Is borne by the National Science Council Taiwan JOURNAL OF BIOMEDICAL SCIENCE RESEARCH Open Access Functional characterization of Trip10 in cancer cell growth and survival 1 1 1 2 1 1 1 Chia-Chen Hsu Yu-Wei Leu Min-Jen Tseng Kuan-Der Lee Tzen-Yu Kuo Jia-Yi Yen Yen-Ling Lai Yi-Chen Hung1 Wei-Sheng Sun1 Chien-Min Chen3 Pei-Yi Chu4 Kun-Tu Yeh4 Pearlly S Yan5 Yu-Sun Chang6 Tim H-M Huang5 Shu-Huei Hsiao1 Abstract Background The Cdc42-interacting protein-4 Trip10 also known as CIP4 is a multi-domain adaptor protein involved in diverse cellular processes which functions in a tissue-specific and cell lineage-specific manner. We previously found that Trip10 is highly expressed in estrogen receptor-expressing ER breast cancer cells. Estrogen receptor depletion reduced Trip10 expression by progressively increasing DNA methylation. We hypothesized that Trip10 functions as a tumor suppressor and may be involved in the malignancy of ER-negative ER- breast cancer. To test this hypothesis and evaluate whether Trip10 is epigenetically regulated by DNA methylation in other cancers we evaluated DNA methylation of Trip10 in liver cancer brain tumor ovarian cancer and breast cancer. Methods We applied methylation-specific polymerase chain reaction and bisulfite sequencing to determine the DNA methylation of Trip10 in various cancer cell lines and tumor specimens. We also overexpressed Trip10 to observe its effect on colony formation and in vivo tumorigenesis. Results We found that Trip10 is hypermethylated in brain tumor and breast cancer but hypomethylated in liver cancer. Overexpressed Trip10 was associated with endogenous Cdc42 and huntingtin in IMR-32 brain tumor cells and CP70 ovarian cancer cells. However overexpression of Trip10 promoted colony formation in IMR-32 cells and tumorigenesis in mice inoculated with IMR-32 cells .

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