<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cai W</submitter><funding>Xiaolong Tang</funding><funding>Wenpeng Cai</funding><pagination>87</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9875405</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Insulin-like growth factor-1 receptor (IGF-1R) promotes cell proliferation and migration and inhibitsapoptosis, all of which can contribute to the development of cancers.&lt;h4>Method&lt;/h4>This study investigated the effect and mechanism of IGF-1R in mediating the desensitization of hepatocellular carcinoma (HCC) to sorafenib.&lt;h4>Results&lt;/h4>IGF-1R, highly expressed in the HCC cell lines SK-Hep1 and HepG2, promotes cell proliferation, migration, and anti-apoptosis through PI3K / Akt and RAS / Raf / ERK signaling pathways, resulting in HCC resistance to sorafenib. Knockdown of IGF-1R by RNA interference decreased proliferation and cell migration and upregulation of sorafenib-induced apoptosis of HCC cells. In vivo studies demonstrated that IGF-1R knockdown inhibited the growt</pubmed_abstract><journal>BMC cancer</journal><pubmed_title>IGF-1R down regulates the sensitivity of hepatocellular carcinoma to sorafenib through the PI3K / akt and RAS / raf / ERK signaling pathways.</pubmed_title><pmcid>PMC9875405</pmcid><funding_grant_id>82071862</funding_grant_id><funding_grant_id>S202110361228</funding_grant_id><pubmed_authors>Song L</pubmed_authors><pubmed_authors>Cao N</pubmed_authors><pubmed_authors>Zhou S</pubmed_authors><pubmed_authors>Ma Y</pubmed_authors><pubmed_authors>Gao J</pubmed_authors><pubmed_authors>Cai W</pubmed_authors><pubmed_authors>Tang X</pubmed_authors></additional><is_claimable>false</is_claimable><name>IGF-1R down regulates the sensitivity of hepatocellular carcinoma to sorafenib through the PI3K / akt and RAS / raf / ERK signaling pathways.</name><description>&lt;h4>Background&lt;/h4>Insulin-like growth factor-1 receptor (IGF-1R) promotes cell proliferation and migration and inhibitsapoptosis, all of which can contribute to the development of cancers.&lt;h4>Method&lt;/h4>This study investigated the effect and mechanism of IGF-1R in mediating the desensitization of hepatocellular carcinoma (HCC) to sorafenib.&lt;h4>Results&lt;/h4>IGF-1R, highly expressed in the HCC cell lines SK-Hep1 and HepG2, promotes cell proliferation, migration, and anti-apoptosis through PI3K / Akt and RAS / Raf / ERK signaling pathways, resulting in HCC resistance to sorafenib. Knockdown of IGF-1R by RNA interference decreased proliferation and cell migration and upregulation of sorafenib-induced apoptosis of HCC cells. In vivo studies demonstrated that IGF-1R knockdown inhibited the growt</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-25T22:36:51.814Z</modification><creation>2025-04-06T09:03:14.529Z</creation></dates><accession>S-EPMC9875405</accession><cross_references><pubmed>36698167</pubmed><doi>10.1186/s12885-023-10561-7</doi></cross_references></HashMap>