{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cai W"],"funding":["Xiaolong Tang","Wenpeng Cai"],"pagination":["87"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9875405"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(1)"],"pubmed_abstract":["<h4>Background</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.<h4>Method</h4>This study investigated the effect and mechanism of IGF-1R in mediating the desensitization of hepatocellular carcinoma (HCC) to sorafenib.<h4>Results</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"],"journal":["BMC cancer"],"pubmed_title":["IGF-1R down regulates the sensitivity of hepatocellular carcinoma to sorafenib through the PI3K / akt and RAS / raf / ERK signaling pathways."],"pmcid":["PMC9875405"],"funding_grant_id":["82071862","S202110361228"],"pubmed_authors":["Song L","Cao N","Zhou S","Ma Y","Gao J","Cai W","Tang X"],"additional_accession":[]},"is_claimable":false,"name":"IGF-1R down regulates the sensitivity of hepatocellular carcinoma to sorafenib through the PI3K / akt and RAS / raf / ERK signaling pathways.","description":"<h4>Background</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.<h4>Method</h4>This study investigated the effect and mechanism of IGF-1R in mediating the desensitization of hepatocellular carcinoma (HCC) to sorafenib.<h4>Results</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","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-25T22:36:51.814Z","creation":"2025-04-06T09:03:14.529Z"},"accession":"S-EPMC9875405","cross_references":{"pubmed":["36698167"],"doi":["10.1186/s12885-023-10561-7"]}}