Open AccessMolecular mechanisms of circular RNAs, transforming growth factor‐ β , and long noncoding RNAs in hepatocellular carcinoma
Author(s) -
Shang Wenkang,
Adzika Gabriel Komla,
Li Yujie,
Huang Qike,
Ding Ningding,
Chinembiri Bianca,
Rashid Mohammad Sajjad Ibn,
Machuki Jeremiah Ong'achwa
Publication year - 2019
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.2553
Subject(s) - long non coding rna , biology , circular rna , hepatocellular carcinoma , cancer research , microrna , signal transduction , transforming growth factor , non coding rna , tumor progression , rna , gene , bioinformatics , microbiology and biotechnology , genetics
At the heart of hepatocellular carcinoma (HCC) lies disruption of signaling pathways at the level of molecules, genes, and cells. Non‐coding RNAs (ncRNAs) have been implicated in the disease progression of HCC. For instance, dysregulated expression of circular RNAs (circRNAs) has been observed in patients with HCC. As such, these RNAs are potential therapeutic targets and diagnostic markers for HCC. Long non‐coding RNAs (lncRNAs), a type of ncRNA, have also been recognized to participate in the initiation and progression of HCC. Transforming growth factor‐beta (TGF‐ β ) is another element which is now recognized to play crucial roles in HCC. It has been implicated in many biological processes such as survival, immune surveillance, and cell proliferation. In HCC, TGF‐ β promotes disease progression by two mechanisms: an intrinsic signaling pathway and the extrinsic pathway. Through these pathways, it modulates various microenvironment factors such as inflammatory mediators and fibroblasts. An interesting yet‐to‐be resolved concept is whether the HCC‐promoting role of TGF‐ β pathways is limited to a subset of HCC patients or it is involved in the whole process of HCC development. This review summarizes recent advancements to highlight the roles of circRNAs, lncRNAs, and TGF‐ β in HCC.