<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kim JY</submitter><funding>National Research Foundation of Korea (NRF)</funding><funding>National Cancer Center</funding><funding>National Cancer Center (NCC)</funding><funding>Korea Health Industry Development Institute</funding><funding>National Research Foundation of Korea</funding><funding>Korea Health Industry Development Institute (KHIDI)</funding><pagination>239</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8924236</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(3)</volume><pubmed_abstract>Ovarian carcinoma (OC) is the most lethal gynecological malignancy due to frequent recurrence resulting from cisplatin-resistance. ARL6IP5 is a novel gene implicated to suppress cisplatin-resistance by activating apoptosis and inhibiting DNA repair through XRCC1 and PARP1. We investigated the clinicopathological and prognostic significance of the immunohistochemical ARL6IP5 expression on 79 post-chemotherapy OC patient tissue samples; in vitro, the effect of ARL6IP5 overexpression (OE) and knockdown (KD) on cancer hallmark functions and the effect of ARL6IP5 on the expression of DNA repair and apoptosis-related proteins were observed in OC cells and their cisplatin-resistant (CisR) counterparts. ARL6IP5 expression was significantly associated with chemotherapeutic response and was an indep</pubmed_abstract><journal>Cell death &amp; disease</journal><pubmed_title>ARL6IP5 reduces cisplatin-resistance by suppressing DNA repair and promoting apoptosis pathways in ovarian carcinoma.</pubmed_title><pmcid>PMC8924236</pmcid><funding_grant_id>2018R1C1B5043725</funding_grant_id><funding_grant_id>2016R1D1A1B03935584</funding_grant_id><funding_grant_id>2019R1FA1059148</funding_grant_id><funding_grant_id>HI21C1137</funding_grant_id><funding_grant_id>NCCCDA2018-04</funding_grant_id><pubmed_authors>Yoon H</pubmed_authors><pubmed_authors>Kim SH</pubmed_authors><pubmed_authors>Kim JY</pubmed_authors><pubmed_authors>Bahar E</pubmed_authors><pubmed_authors>Kim HS</pubmed_authors><pubmed_authors>Park EY</pubmed_authors><pubmed_authors>Do SI</pubmed_authors><pubmed_authors>Chang S</pubmed_authors><pubmed_authors>Lee JY</pubmed_authors></additional><is_claimable>false</is_claimable><name>ARL6IP5 reduces cisplatin-resistance by suppressing DNA repair and promoting apoptosis pathways in ovarian carcinoma.</name><description>Ovarian carcinoma (OC) is the most lethal gynecological malignancy due to frequent recurrence resulting from cisplatin-resistance. ARL6IP5 is a novel gene implicated to suppress cisplatin-resistance by activating apoptosis and inhibiting DNA repair through XRCC1 and PARP1. We investigated the clinicopathological and prognostic significance of the immunohistochemical ARL6IP5 expression on 79 post-chemotherapy OC patient tissue samples; in vitro, the effect of ARL6IP5 overexpression (OE) and knockdown (KD) on cancer hallmark functions and the effect of ARL6IP5 on the expression of DNA repair and apoptosis-related proteins were observed in OC cells and their cisplatin-resistant (CisR) counterparts. ARL6IP5 expression was significantly associated with chemotherapeutic response and was an indep</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-22T18:17:50.905Z</modification><creation>2025-04-06T02:24:48.333Z</creation></dates><accession>S-EPMC8924236</accession><cross_references><pubmed>35293383</pubmed><doi>10.1038/s41419-022-04568-4</doi></cross_references></HashMap>