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MutY-Homolog (MYH) inhibition reduces pancreatic cancer cell growth and increases chemosensitivity


Patients with pancreatic ductal adenocarcinoma (PC) have a poor prognosis due to metastases and chemoresistance. PC is characterized by extensive fibrosis, which creates a hypoxic microenvironment, and leads to increased chemoresistance and intracellular oxidative stress. Thus, proteins that protect against oxidative stress are potential therapeutic targets for PC. A key protein that maintains genomic integrity against oxidative damage is MutY-Homolog (MYH). No prior studies have investigated the function of MYH in PC cells. Using siRNA, we showed that knockdown of MYH in PC cells 1) reduced PC cell proliferation and increased apoptosis; 2) further decreased PC cell growth in the presence of oxidative stress and chemotherapy agents (gemcitabine, paclitaxel and vincristine); 3) reduced PC cell metastatic potential; and 4) decreased PC tumor growth in a subcutaneous mouse model in vivo. The results from this study suggest MYH may be a novel therapeutic target for PC that could potentially improve patient outcome by reducing PC cell survival, increasing the efficacy of existing drugs and reducing metastatic spread.

Type Journal
ISBN 1949-2553 (Electronic) 1949-2553 (Linking)
Authors Sharbeen, G.; Youkhana, J.; Mawson, A.; McCarroll, J.; Nunez, A.; Biankin, A.; Johns, A.; Goldstein, D.; Phillips, P.
Responsible Garvan Author Amber Johns
Publisher Name Oncotarget
Published Date 2017-02-07
Published Volume 8
Published Issue 6
Published Pages 9216-9229
Status Published in-print
DOI 10.18632/oncotarget.13985
URL link to publisher's version
OpenAccess link to author's accepted manuscript version