期刊
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
卷 1876, 期 1, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.bbcan.2021.188574
关键词
HCC; STAT3; Noncoding RNAs; Oncogenic; Tumor suppressor; Molecular sponging; ceRNA
资金
- Council of Scientific & Industrial Research
- University Grants Commission, New Delhi
- NUHS Seed Fund
Hepatocellular carcinoma (HCC) is a deadly cancer with a high mortality rate, and STAT3 plays a crucial role in its development by regulating various genes and cellular functions. Long noncoding RNAs (lncRNAs) influence STAT3 signaling through diverse molecular mechanisms, impacting the pathogenesis and progression of HCC.
Hepatocellular carcinoma (HCC) is one of the lethal and leading types of cancer threatening the globe with a high mortality rate. STAT3 is an oncogenic transcription factor that is aberrantly activated in several human malignancies including HCC. Many STAT3-driven genes control cell proliferation and survival, apoptotic resistance, cell cycle progression, metastasis, and chemotherapeutic resistance. STAT3 signaling is regulated by endogenous modulators such as protein tyrosine phosphatase (PTP), suppressor of cytokine signaling (SOCS), protein inhibitor of activated STAT (PIAS), and various long noncoding RNAs (lncRNAs). Interestingly, lncRNAs have been reported to exhibit oncogenic and tumor suppressor functions, and these effects are mediated through diverse molecular mechanisms including sponging of microRNAs (miRs), transcription activation/inhibition, and epigenetic modifications. In this article, we have discussed the possible role of STAT3 signaling in hepatocarcinogenesis and various mechanisms by which lncRNAs impart their oncogenic or tumor suppressive action by modulating the STAT3 pathway in HCC.
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