{
"@context": "http://schema.org",
"@type": "ScholarlyArticle",
"@id": "https://doi.org/10.6084/m9.figshare.18544557",
"url": "https://tandf.figshare.com/articles/journal_contribution/Long_intergenic_non-protein_coding_RNA_1273_confers_sorafenib_resistance_in_hepatocellular_carcinoma_via_regulation_of_methyltransferase_3/18544557",
"additionalType": "Journal contribution",
"name": "Long intergenic non-protein coding RNA 1273 confers sorafenib resistance in hepatocellular carcinoma via regulation of methyltransferase 3",
"author": [
{
"name": "Huifang Kong",
"givenName": "Huifang",
"familyName": "Kong"
},
{
"name": "Jie Sun",
"givenName": "Jie",
"familyName": "Sun"
},
{
"name": "Wei Zhang",
"givenName": "Wei",
"familyName": "Zhang"
},
{
"name": "Huixin Zhang",
"givenName": "Huixin",
"familyName": "Zhang"
},
{
"name": "Hong Li",
"givenName": "Hong",
"familyName": "Li"
}
],
"description": "Hepatocellular carcinoma (HCC) is often diagnosed in patients with advanced disease who are ineligible for curative surgical therapies. Sorafenib is a first-line agent approved for the treatment of advanced HCC. However, the frequent resistance of HCC cells to sorafenib greatly reduces its efficacy. Herein, we describe a novel long non-coding RNA (lncRNA) conferring sorafenib resistance. Long intergenic non-protein coding RNA 1273 (LINC01273) was significantly overexpressed in human HCC and sorafenib-resistant tissues, linking it to poor overall and relapse-free survival. We established sorafenib-resistant Huh7 (Huh7-SR) and SMMC-7721 (SMMC-7721-SR) cells, and found that the knockdown of LINC01273 repressed the viability, colony formation, and DNA synthesis rate of Huh7-SR and SMMC-7721-SR cells. The level of N6-methyladenosine (m6A) in sorafenib-resistant HCC cells was significantly decreased, which was rescued by LINC01273 silencing. Mechanistically, LINC01273 complementarity bound to miR-600, served as a ‘reservoir’ increasing miR-600 stability, and facilitating miR-600 targeting methyltransferase 3 (METTL3), a m6A ‘writer’, resulting in reducing METTL3 level. In addition, LINC01273 was modified with m6A, METTL3 increased LINC01273 m6A modification, followed by LINC01273 decay in the presence of YTHDF2, a m6A ‘reader’. Our findings reveal the key role of LINC01273 in sorafenib-resistant HCC cells, and targeting of the newly identified LINC01273/miR-600/METTL3 feedback regulatory axis may be a promising effective intervention for HCC patients with sorafenib resistance.",
"license": "https://creativecommons.org/licenses/by/4.0/legalcode",
"keywords": "Biophysics, Medicine, Cell Biology, Genetics, FOS: Biological sciences, Molecular Biology, Biological Sciences not elsewhere classified, Cancer, Hematology, Infectious Diseases, FOS: Health sciences, Virology",
"contentSize": "11436132 Bytes",
"dateCreated": "2022-01-17",
"datePublished": "2022",
"dateModified": "2024-03-21",
"@reverse": {
"isBasedOn": {
"@id": "https://doi.org/10.1080/21655979.2022.2025701",
"@type": "ScholarlyArticle"
}
},
"schemaVersion": "http://datacite.org/schema/kernel-4",
"publisher": {
"@type": "Organization",
"name": "Taylor & Francis"
},
"provider": {
"@type": "Organization",
"name": "datacite"
}
}