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Contribution and underlying mechanisms of lncRNA TRPM2-AS in the development and progression of human cancers.
Li, Fei; Chen, Xiuwei.
Afiliação
  • Li F; Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, Heilongjiang 150081, China.
  • Chen X; Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin Medical University, Harbin, Heilongjiang 150081, China. Electronic address: 1427@hrbmu.edu.cn.
Pathol Res Pract ; 251: 154887, 2023 Nov.
Article em En | MEDLINE | ID: mdl-37871443
ABSTRACT
Long-stranded non-coding RNAs (lncRNAs) are RNA molecules that are longer than 200 nucleotides and do not code for proteins. They play a significant role in various biological processes, including epigenetics, cell cycle, and cell differentiation. Many studies have shown that the occurrence of human cancer is closely related to the abnormal expression of lncRNA. In recent years, lncRNAs have been a hot topic in cancer research. TRPM2-AS, a novel lncRNA, is aberrantly expressed in many human cancers, and its overexpression is strongly linked to poor clinical outcomes in patients. It has been demonstrated that TRPM2-AS acts as a ceRNA, participates in signaling pathways, and interacts with biological proteins and other molecular mechanisms to regulate gene expression. In addition, it can regulate the proliferation, migration, invasion, apoptosis, and treatment resistance of cancer cells. As a result, TRPM2-AS may be a potential target for cancer treatment and a possible biomarker for cancer prognosis. This review outlined the expression, biological processes, and molecular mechanisms of TRPM2-AS in various malignancies, and discussed potential therapeutic uses.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Canais de Cátion TRPM / RNA Longo não Codificante / Neoplasias Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Canais de Cátion TRPM / RNA Longo não Codificante / Neoplasias Limite: Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article