Title

野生型及Thr^187突變型p27(上標 Kip1)蛋白對HepG2細胞週期的影響

Translated Titles

Over-expression of p27(superscript Kip1) Threonine Residue 187 Mutant Type Gene Induces G0 Phase Arrest in HepG2 Cell Lines

Authors

管曉翔(Xiao-Xiang Guan);陳龍邦(Long-Bang Chen);王靖華(Jing-Hua Wang);耿懷成(Huai-Cheng Geng);褚曉源(Xiao-Yuan Chu);張群(Qun Zhang);鹿紅(Hong Lu);林勍(Qing Lin)

Key Words

腫瘤細胞 ; 細胞轉染 ; 細胞週期 ; p27(上標 kip1) ; carcinoma cell ; transfection ; cell cycle ; p27(superscript Kip1)

PublicationName

南京醫科大學學報(自然科學版)

Volume or Term/Year and Month of Publication

24卷5期(2004 / 09 / 05)

Page #

449 - 451

Content Language

簡體中文

Chinese Abstract

Objective: To evaluate the effects of p27(superscript Kip1) transfection on the cell cycle, we transfected HepG2 lines with a high activity of p27(superscript Kip1) threonine 187-to-alanine (T187A) mutant gene as well as with wild type gene, then to investigate the role of phosphorylation of Thr^187 of p27(superscript Kip1) protein in its subcellular localization and cell cycle and proliferation. Methods: We transfected p27(superscript Kip1) T187A mutant and wild type gene into HepG2 cell lines by using Lipofectamine (LF2000) separately. The exogenous p27(superscript Kip1) protein expression and subcellular localization were monitored with immunoflurescence microscopy. FACS and growth curves were used to analyse its biological effects on cell cycle and proliferation. Results: Over-expression of p27(superscript Kip1) protein inhibited cell growth and increased cell number at the G1 phase. Moreover, transfection of the T187A mutant gene was more effective in inhibiting cell growth. Conclusion: The over-expression of p27(superscript Kip1) maybe inhibit the proliferation of HepG2, deletion of p27(superscript Kip1) on Thr187 may be beneficial to tumor cell G0 arrest, and these results suggest that the transfection of the p27(superscript Kip1) T187A mutant gene can be a modality of cancer gene therapy target.

English Abstract

Objective: To evaluate the effects of p27(superscript Kip1) transfection on the cell cycle, we transfected HepG2 lines with a high activity of p27(superscript Kip1) threonine 187-to-alanine (T187A) mutant gene as well as with wild type gene, then to investigate the role of phosphorylation of Thr^187 of p27(superscript Kip1) protein in its subcellular localization and cell cycle and proliferation. Methods: We transfected p27(superscript Kip1) T187A mutant and wild type gene into HepG2 cell lines by using Lipofectamine (LF2000) separately. The exogenous p27(superscript Kip1) protein expression and subcellular localization were monitored with immunoflurescence microscopy. FACS and growth curves were used to analyse its biological effects on cell cycle and proliferation. Results: Over-expression of p27(superscript Kip1) protein inhibited cell growth and increased cell number at the G1 phase. Moreover, transfection of the T187A mutant gene was more effective in inhibiting cell growth. Conclusion: The over-expression of p27(superscript Kip1) maybe inhibit the proliferation of HepG2, deletion of p27(superscript Kip1) on Thr187 may be beneficial to tumor cell G0 arrest, and these results suggest that the transfection of the p27(superscript Kip1) T187A mutant gene can be a modality of cancer gene therapy target.

Topic Category 醫藥衛生 > 醫藥衛生綜合
醫藥衛生 > 藥理醫學