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Effect of fragile histidine triad gene transduction on proliferation and apoptosis of human hepatocellular carcinoma cells

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World Journal of Gastroenterology 2008年第23期14卷 3754-3758页

作者： Rong-Hua Xu Liang-Yan Zheng Dong-Lei He Jian Tong Li-Ping Zheng Wu-Ping Zheng Jin Meng Li-Ping Xia Cong-Jun Wang Ji-Lin Yi The Affiliated Hospital of Hainan Medical College Haikou 570102 Hainan Province China Department of general Surgery First People's Hospital Affiliated to Shanghai Jiaotong University Shanghai 200080 China Department of general surgery Tongji Hospital Tongji Medical College of Huazhong University of Science and Technology Wuhan 430030 Hubei Province China

AIM:To evaluate the inhibitory effects of human fragile histidine triad(FHIT) gene on cell proliferation and apoptosis in human hepatocellular carcinoma line Hep3B in vitro. METHODS:A recombinant pcDNA3.1(+) /FHIT including the functional region of FHIT gene was constructed and transferred into human hepatocellular carcinoma cells in vitro. mRNA and protein expression of the FHIT gene in the transfected cells was detected by RT-PCR and Western blot,respectively. The effect of FHIT on proliferation was detected by MTT assay. Changes in cell cycle and apoptosis were assayed by flow cytometry. Five mice received subcutaneous transplantation of Hep3B-FHIT;5 mice received subcutaneous transplantation of normal Hep3B and Hep3B-C as controls. The body weight of nude mice and tumor growth were measured. RESULTS:RT-PCR and Western blot analysis showed that the expression level of FHIT-mRNA and FHIT protein was higher in Hep3B cells after infection withpcDNA3.1(+) /FHIT. The growth of Hep3B cells treated with pcDNA3.1(+) /FHIT was significantly inhibited. The pcDNA3.1(+) /FHIT-transfected Hep3B cells showed a significantly higher cell rate at G0-G1 phase and increased apoptosis in comparison with controls(P gene inhibits the growth of human hepatocellular carcinoma cells and induces cell apoptosis in vivo and in vitro.

关键词： Hepatocellular carcinoma gene therapy fragile histidine triad gene

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Expression of Ki-67, galectin-3, fragile histidine triad, and parafibromin in malignant and benign parathyroid tumors

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Chinese Medical Journal 2012年第16期125卷 2895-2901页

作者： WANG Ou WANG Chun-yan SHI Jie NIE Min XIA Wei-bo LI Mei JIANG Yan GUAN Heng MENG Xun-wu XING Xiao-ping Key Laboratory of Endocrine Ministry of HealthDepartment of EndocrinologyPeking Union Medical College HospitalPeking Union Medical College&Chinese Academy of Medical SciencesBeijing 100730China Department of Pathology Peking Union Medical College Hospital Peking Union Medical College&Chinese Academy of Medical SciencesBeijing 100730China Department of Surgery Peking Union Medical College HospitalPeking Union Medical College&Chinese Academy of Medical SciencesBeijing 100730China Department of Endocrinology Aviation General HospitalBeijing 100012China

Background It is widely recognized that the diagnosis of parathyroid carcinoma （PC） is often difficult because of the overlap of characteristics between malignant and benign parathyroid tumors, especially at an early stage. Our study aimed to investigate the differential expression of Ki-67, galectin-3, fragile histidine triad （FHIT） gene, and parafibromin in PC, parathyroid adenoma （PA）, parathyroid hyperplasia （PH）, and normal parathyroid （NP） tissues; then to assess these expression values for use in differential diagnosis of malignant and benign parathyroid tumors. Methods Data of 15 cases with PC, 19 PAs, and 8 PHs were retrospectively analyzed for their clinical characteristics. The expression of Ki-67, galectin-3, FHIT, and parafibromin were detected via immunohistochemistry in the above-mentioned specimens and 6 NPs as control. Results Complete loss of parafibromin expression was seen in 9 of 15 （60%） carcinomas, and all normal parathyroid tissues and parathyroid benign tumors stained positive for parafibromin except for one （4%） adenoma. Galectin-3 staining was positive in 11 of 15 （73%） carcinomas, 5 of 19 （26%） adenomas, 1 of 8 （12%） hyperplasias, and 0 of 6 normal tissues. The Ki-67 proliferative index was high in 4 of 15 （27%） carcinomas, 1 of 19 （5%） adenomas, and none of the hyperplasia or normal tissues. FHIT expression did not differ appreciably among the tumor types. The combination of overexpression of galectin-3 or loss of parafibromin increased sensitivity for PC to 87%, while the specificity of both positive galectin-3 and positive Ki-67 could reach 100%. Conclusions These data suggested that loss of parafibromin and overexpression of galectin-3 and Ki-67 might help to distinguish parathyroid carcinoma from other parathyroid tumors. And the combination of two or three of these markers might produce better sensitivity and/or specificity for the diagnosis of parathyroid carcinoma.

关键词： parathyroid tumors, Ki-67, galectin-3 parafibromin fragile histidine triad gene

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