MicroRNA‐122 suppresses cell proliferation and induces cell apoptosis in hepatocellular carcinoma by directly targeting Wnt/β‐catenin pathway

Abstract

MiR-122 expression is down-regulated in human HCC. Over-expression of miR-122 inhibits HCC cell growth and promotes the cell apoptosis by affecting Wnt/β-catenin-TCF signalling pathway.

Retracted: MicroRNA‐140‐5p elevates cerebral protection of dexmedetomidine against hypoxic–ischaemic brain damage via the Wnt/β‐catenin signalling pathway

“…Wnt1 has been proven to protect against neuronal injury, protein of which significantly increases neuronal cell survival 28. Furthermore, β‐catenin with TCF could activate some specific target genes related to cell apoptosis, and increased TCF‐4 mRNA expression is helpful for survival of breast cancer patients 29. Consistent with the aforementioned finding, a previous study asserted that overexpressed β‐catenin could inhibit apoptosis induced by hypoxia through the HIF‐1α signalling, suggesting that mRNA and protein expression of β‐catenin and TCF‐4 may be up‐regulated in HIBD rats 30…”

MicroRNA-122 Promotes Proliferation, Invasion and Migration of Renal Cell Carcinoma Cells Through the PI3K/Akt Signaling Pathway

“…Overexpression of miR-122 could suppress proliferation and induce apoptosis and cell cycle arrest in cancer cells through reducing the expression of Bcl-W, CCNG1 (Ma et al, 2010), IGF1R/PI3K/Akt (Wang et al, 2012) and Wnt/beta-catenin signal pathways (Xu et al, 2012). These findings suggest that miR-122 may behave as a tumor suppressor in hepatocellular carcinoma and breast cancers.…”

MiR-122 in hepatic function and liver diseases

“…Loss of miR-122 facilitates cell tumorigenic properties such as cell migration and invasion, and restoration of miR-122 reverses this phenotype. Currently, several target genes of miR-122 have been identified to be involved in hepatocarcinogenesis, such as ADAM10 (a distintegrin and metalloprotease family 10), serum response factor (SRF) (Bai et al, 2009), insulin-like growth factor 1 receptor (Igf1R) (Zeng et al, 2010), cyclin G1 (Fornari et al, 2009), and Wnt1 (Xu et al, 2012). In addition, overexpression and restoration of miR-122 in HCC cells has been shown to sensitize HCC cells to chemotherapeutic agents (Bai et al, 2009;Xu et al, 2011;Yang et al, 2011).…”