ENTPD5 induces apoptosis in lung cancer cells via regulating caspase 3 expression

PloS One
Yijun XueJinfeng Chen

Abstract

This study is to investigate the relationship between ectonucleoside triphosphate diphosphohydrolase 5 (ENTPD5) expression and lung cancer clinicopathological factors, and the impact of ENTPD5 on lung cancer cell functions. Lung cancer specimens and matched adjacent normal tissues were obtained from patients without any preoperative radiotherapy or chemotherapy. Knockdown of ETNPD5 expression led to significantly decreased lung cancer cell growth rate, markedly increased apoptosis and the ability to repair, and significantly reduced invasion. Gene chip tests showed that knockdown of ENTPD5 expression caused more Caspase expression. Quantitative real-time polymerase chain reaction showed that the Caspase 3 expression was significantly increased after the knockdown of ENTPD5. In addition, immunohistochemistry showed that the tumor growth marker, proliferating cell nuclear antigen, was significantly reduced in the knockdown model. Tumorigenicity assay and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay showed that the apoptosis of lung cancer cells was increased in the knockdown model. Our results suggest that ENTPD5 affects lung cancer apoptosis via Caspase 3 pathway, and can be potentially used to mon...Continue Reading

References

Jan 27, 2000·Cell·D Hanahan, R A Weinberg
Oct 13, 2001·European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)·R I NicholsonM E Harper
May 11, 2002·Nature Reviews. Cancer·Frederik H Igney, Peter H Krammer
Dec 19, 2002·Molecular Carcinogenesis·María José BlánquezVicente Notario
Sep 15, 2004·Lung Cancer : Journal of the International Association for the Study of Lung Cancer·Vienna LudoviniMaurizio Tonato
Jun 7, 2005·Lung Cancer : Journal of the International Association for the Study of Lung Cancer·Seok Jin KimMichael J Kelley
Feb 14, 2006·Head & Neck·Dirk R BuitelaarJohannes M Huitink
Sep 14, 2006·European Journal of Cancer Care·K AlzahouriF Guillemin
Sep 21, 2012·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Sohila ZadranHomera Zadran
Aug 8, 2013·International Journal of Oncology·Caitlin M MacCarthy, Vicente Notario
Apr 5, 2014·Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire·Aline BeckenkampAndréia Buffon
Aug 28, 2014·Expert Review of Respiratory Medicine·Nanda Horeweg, Harry de Koning

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Citations

Jan 1, 2021·Cancers·János Tibor FeketeBalázs Győrffy
Jun 3, 2021·Purinergic Signalling·Rafael Paschoal de CamposGuido Lenz

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Methods Mentioned

BETA
electrophoresis
fluorescence microscopy
transfection
flow cytometry
chip

Software Mentioned

SPSS
CellQuest Pro

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