Histone Deacetylases Inhibit the Snail2-Mediated EMT During Metastasis of Hepatocellular Carcinoma Cells

Abstract

Snail2 has an important role in the epithelial-mesenchymal transition (EMT) and tumor metastasis. Here, we report that Snail2 is highly expressed during TGF-β induced EMT in HL-7702 cells. Additionally, overexpression of Snail2 successfully promotes the migration and invasion of these cells, both in vitro and in a mouse model. Furthermore, our results show that HDAC1 and HDAC3 could suppress the Snail2 gene promoter. Moreover, we find that the acetylation of H3K4 and H3K56 are significantly reduced during the EMT process of liver HL-7702 cells. Thus, our results indicate that HDAC1 and HDAC3 epigenetically suppress the expression of Snail2 during the EMT of liver cells, revealing an opposing function of HDACs during the migration of malignant tumors.

Hepigenetics: A Review of Epigenetic Modulators and Potential Therapies in Hepatocellular Carcinoma

“…Interestingly, HDACs were also shown to counter cell migration. Acetylation of H3K4 and H3K56 within the Snail2 promoter was markedly reduced in EMT thanks to HDAC1 and HDAC3 [ 70 ]. It is worthy to note that G9a, a histone H3 lysine 9 (H3K9) methyltransferase, has been recently recognized as vital for such Snail2 -mediated inhibition of E-cadherin and consequent repression of mesenchymal properties [ 71 ].…”

Construction and Validation of a Prognostic Risk Model Based on Autophagy-Related Genes in Hepatocellular Carcinoma Cells

“…Silencing of HDAC1 enhances the sensitivity of ovarian cancer to chemotherapy 21 . HDAC1 restrains Snail2-mediated epithelial-mesenchymal transition (EMT) in the process of metastasis of HCC (Yue Hu et al 22 ). Viewed in toto, these genes participate in progression of HCC, which is consistent with this paper.…”

Low-dose naltrexone plays antineoplastic role in cervical cancer progression through suppressing PI3K/AKT/mTOR pathway

“…Scratch assays were performed as described previously [19] , [20] . Before the scratch assay, the medium of each cell group treated with LDN was replaced with a serum-free medium and cultured for 1 h. The wound scratch was created using a 200 μl pipette tip on the cell surface of the Petri dish, which was then washed once with serum-free medium.…”