<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Peng DJ</submitter><funding>NCI NIH HHS</funding><funding>NIH</funding><pagination>600-5</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4063277</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>394(3)</volume><pubmed_abstract>The mechanism of cisplatin resistance in cancer cells is not fully understood. Here, we show that the Akt/mTOR survival pathway plays an important role in cisplatin resistance in human ovarian cancer cells. Specifically, we found that cisplatin treatment activates the Akt/mTOR survival pathway and that inhibition of this pathway by the PI3K inhibitor LY294002 or knockdown of Akt sensitizes ovarian cancer cells to cisplatin. Furthermore, we generated cisplatin-resistant cells and found that resistant cells express a higher level of activated Akt as compared to their cisplatin sensitive counterparts. Importantly, inhibition of Akt or mTOR sensitized resistant cells to cisplatin-induced apoptosis. Taken together, our data indicate that activation of the Akt/mTOR pathway prevents cisplatin-ind</pubmed_abstract><journal>Biochemical and biophysical research communications</journal><pubmed_title>Role of the Akt/mTOR survival pathway in cisplatin resistance in ovarian cancer cells.</pubmed_title><pmcid>PMC4063277</pmcid><funding_grant_id>R01 CA100073</funding_grant_id><pubmed_authors>Peng DJ</pubmed_authors><pubmed_authors>Zhou JY</pubmed_authors><pubmed_authors>Wu GS</pubmed_authors><pubmed_authors>Wang J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of the Akt/mTOR survival pathway in cisplatin resistance in ovarian cancer cells.</name><description>The mechanism of cisplatin resistance in cancer cells is not fully understood. Here, we show that the Akt/mTOR survival pathway plays an important role in cisplatin resistance in human ovarian cancer cells. Specifically, we found that cisplatin treatment activates the Akt/mTOR survival pathway and that inhibition of this pathway by the PI3K inhibitor LY294002 or knockdown of Akt sensitizes ovarian cancer cells to cisplatin. Furthermore, we generated cisplatin-resistant cells and found that resistant cells express a higher level of activated Akt as compared to their cisplatin sensitive counterparts. Importantly, inhibition of Akt or mTOR sensitized resistant cells to cisplatin-induced apoptosis. Taken together, our data indicate that activation of the Akt/mTOR pathway prevents cisplatin-ind</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Apr</publication><modification>2025-05-29T15:58:48.38Z</modification><creation>2025-05-29T15:58:48.38Z</creation></dates><accession>S-EPMC4063277</accession><cross_references><pubmed>20214883</pubmed><doi>10.1016/j.bbrc.2010.03.029</doi></cross_references></HashMap>