Overexpression of PHRF1 attenuates the proliferation and tumorigenicity of non-small cell lung cancer cells.
The aim of this study was to investigate the potential role of PHRF1 in lung tumorigenesis. Western blot analysis was used to detect the expression of proteins. Quantitative reverse transcriptase polymerase chain reaction, immunohistochemistry, soft agar assay and tumor formation assay in nude mice were applied. Cell cycle distribution was analyzed by flow cytometry. The lower level of PHRF1 mRNA was observed in human lung cancer tissues than that in paracancerous tissues. The decreased expression of PHRF1 protein was observed in H1299 and H1650 cell lines than that in 16HBE and BEAS-2B cell lines. The decreased expression of PHRF1 protein was observed in malignant 16HBE cells compared to control cells. The reduced expression of PHRF1 protein was observed in mice lung tissues treated with BaP than that in control group. Overexpression of PHRF1 inhibited H1299 cell proliferation, colony formation in vitro and growth of tumor xenograft in vivo, and arrested cell cycle in G1 phase. The decreased expression of TGIF and c-Myc proteins and the increased expression of p21 protein were observed in H1299-PHRF1 cells compared with H1299-pvoid cells. In conclusion, our findings suggest that overexpression of PHRF1 attenuated the proliferation and tumorigenicity of non-small cell lung cancer cell line of H1299.
Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou 450016, China.|Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, Xinxiang Medical University, Xinxiang 453003, China.
Yadong
Y
Wang
Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou 450016, China.
Haiyu
H
Wang
Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou 450001, China.
Teng
T
Pan
Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou 450016, China.
Li
L
Li
Department of Toxicology, Henan Center for Disease Control and Prevention, Zhengzhou 450016, China.
Jiangmin
J
Li
Department of Epidemiology, School of Public Health, Zhengzhou University, Zhengzhou 450001, China.
Haiyan
H
Yang
D000818:Animals; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D059585:G1 Phase Cell Cycle Checkpoints; D015972:Gene Expression Regulation, Neoplastic; D018398:Homeodomain Proteins / Q000378:metabolism; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008819:Mice, Nude; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D012097:Repressor Proteins / Q000378:metabolism; D015398:Signal Transduction; D013997:Time Factors; D047368:Tumor Burden; D015854:Up-Regulation
C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D018398:Homeodomain Proteins; C489427:MYC protein, human; D008565:Membrane Proteins; C000626148:PHD and RING finger domain-containing protein 1, human; D016271:Proto-Oncogene Proteins c-myc; D012097:Repressor Proteins; C097504:TGIF1 protein, human
H1299 cell; PHRF1; cell cycle; lung cancer; tumorigenicity