The Effects of HSP27 on Gemcitabine-Resistant Pancreatic Cancer Cell Line Through Snail

Pancreas
Song ZhangXiao-Ping Zou

Abstract

To evaluate the regulation mechanism of heat shock protein 27 (HSP27) on gemcitabine (GEM) resistance of pancreatic cancer cell. The expression vectors pEGFP-C1-HSP27 and the vectors of MicroRNA targeting Snail were introduced into GEM-sensitive pancreatic cancer SW1990 cells, and the vectors of small hairpin RNA targeting HSP27 were transfected into SW1990 and GEM-resistant SW1990/GEM cells. The expressions of HSP27, p-HSP27 (Ser82), Snail, ERCC1, and E-cadherin were evaluated by Western blotting. The sensitivity of transfected cells to GEM was detected by CCK-8 assay and Annexin V-FITC apoptosis assay. As compared to SW1990, SW1990/GEM showed significantly increased expressions of HSP27, p-HSP27, Snail and ERCC1 with decreased expression of E-cadherin. By increasing HSP27 expression, we found increase of Snail and ERCC1 with reduction of E-cadherin expressions, while reduction of HSP27 expression caused reduction of Snail and ERCC1 but increase of E-cadherin expressions. Downregulation of Snail resulted in the reduction of ERCC1 expression and increase of E-cadherin. Furthermore, downregulation of HSP27 or snail caused increased GEM sensitivity of pancreatic cancer cells, and upregulation of HSP27 showed the opposite results....Continue Reading

References

Apr 10, 1999·Genes & Development·W L de LaatJ H Hoeijmakers
Sep 26, 2000·Molecular and Cellular Biology·S J CharetteJ Landry
May 24, 2001·Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract·R A Abrams
Jan 11, 2002·Molecular and Cellular Biology·Catherine PaulAndré-Patrick Arrigo
Aug 22, 2002·Nature Reviews. Cancer·Jean Paul Thiery
Oct 23, 2004·The British Journal of Surgery·N AlexakisJ P Neoptolemos
Feb 12, 2005·Antioxidants & Redox Signaling·Arnaud ParcellierCarmen Garrido
Apr 6, 2006·Cancer Causes & Control : CCC·Rosemary D CressElizabeth A Holly
Jun 23, 2007·The Journal of Surgical Research·Tao YinMing Yang
Oct 3, 2007·Annals of Surgical Oncology·Ami N ShahGary E Gallick
Dec 20, 2007·Cancer Research·Cornelia O'Callaghan-SunolMichael Y Sherman
May 17, 2008·Cancer Research·Tamer T OnderRobert A Weinberg
Jul 23, 2008·Current Genomics·Alan SoMartin Gleave
Jul 9, 2009·Cancer Research·Thiruvengadam ArumugamWoonyoung Choi
Dec 8, 2009·Clinical Chemistry and Laboratory Medicine : CCLM·Qiaojia HuangXu Lin
Dec 29, 2009·FEBS Letters·Nan Chen, Jayanta Debnath
Apr 9, 2010·Journal of Innate Immunity·Anne-Laure JolyCarmen Garrido
Jul 9, 2010·CA: a Cancer Journal for Clinicians·Ahmedin JemalElizabeth Ward
Sep 9, 2010·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Dennis Shin-Shian HsuMuh-Hwa Yang
May 25, 2011·Biochimica Et Biophysica Acta·Ashraf A KhalilChristopher Smith
Oct 19, 2011·Journal of Cellular and Molecular Medicine·Claus SchäferEike Gallmeier

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Citations

Jan 26, 2016·International Journal of Molecular Sciences·Mitsuru OkunoIchiro Yasuda
Apr 24, 2021·International Immunopharmacology·Yuanjie LiHanqing Wang

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