MicroRNA-520d-3p suppresses melanoma cells proliferation by inhibiting the anti-silencing function 1B histone chaperone

Abstract

As the most common and aggressive malignant form of skin cancer, melanoma has a poor prognosis in its late stage. MicroRNA (miR)-520d-3p has been reported as a key modulator that regulates the development of different types of cancer, but its role in melanoma remains unclear. The purpose of this study was to investigate the role and mechanism of miR-520d-3p in melanoma. The expression of anti-silencing function 1B histone chaperone ( ASF1B ) and miR-520d-3p in melanoma tissues and cells was detected by reverse transcription-quantitative polymerase chain reaction. The interaction between ASF1B and miR-520d-3p was verified by luciferase activity detection. Cell counting kit-8, bromodeoxyuridine, fluorescein isothiocyanate, and cell adhesion assays were performed to detect cell viability, proliferation, apoptosis, and adhesion in melanoma cells. ASF1B expression was evidently increased, whereas miR-520d-3p level was downregulated in melanoma tissues and cells. Overexpression of ASF1B enhanced cell growth and adhesion and hampered cell apoptosis in melanoma cells. Furthermore, miR-520d-3p suppressed the tumorigenic effects of melanoma cells. Moreover, miR-520d-3p suppressed the expression of ASF1B to suppress melanoma tumorigenesis. In conclusion, we have found out that miR-520d-3p suppressed melanoma tumorigenesis by inhibiting ASF1B , which could be a promising target for melanoma therapy.

MiR-520d-3p suppresses the proliferation and epithelial-mesenchymal transition of cervical cancer cells by targeting ZFP36L2

“…Data from in vitro assays indicated that overexpression of miR-520d-3p inhibited proliferation and migration of HeLa and SiHa cells. In agreement with our data, restoration of miR-520d-3p expression reduced cell viability by causing the accumulation of cell apoptosis in breast cancer [ 15 ] and melanoma [ 17 ]. Upregulation of miR-520d-3p dramatically inhibited the cell proliferation, migration and invasion of gastric cancer [ 13 ] and hepatocellular carcinoma [ 16 ].…”

“…Overexpression of miR-520d-3p showed a significant inhibitory effect on cell proliferation and accompanied cell cycle G0/G1 arrest in glioma cells [ 14 ]. In addition, miR-520d-3p exerted suppressive effects on cell proliferation and migration in breast cancer [ 15 ], hepatocellular carcinoma [ 16 ] and melanoma [ 17 ]. However, the functional role of miR-520d-3p in CC and its mechanism of action have not been reported yet.…”

Identification of ASF1B as a prognostic marker for liver cancer by meta-analysis and its immune value revealed by a comprehensive pan-cancer analysis of 33 human cancers

“…The establishment of a multi-molecular biological prediction model of liver cancer has very important clinical significance for improving the treatment effect and prognosis [ 4 , 16 ]. The ASF1B gene is located on chromosome 19q13.12 and consists of 4 exons that regulate the nucleosome structure of chromatin by encoding members of the histone chaperone H3/H4 family, and providing histones to nucleosome assembly sites plays a key role in [ 8 , 17 , 18 ]. It has been reported that ASF1A and ASF1B in humans can co-deplete the alternately elongated telomere (ALT) pathway maintained at the ends of mammalian chromosomes in primary cells and cancer cells [ 19 ].…”

“…The ASF1b protein, a substrate of the tangle-like kinase family of cell cycle-regulated protein kinases, plays a key role in regulating the nucleosomal structure of chromatin through the continuous supply of histones to the site of nucleosome assembly, while also participating in the role of transcriptional regulators [7]. Previous studies have shown that ASF1B affects the pathogenesis of cancers such as cervical cancer, prostate cancer, and clear cell renal cell carcinoma, and it can enhance tumour cell growth and migration [8][9][10]. Another study reported the role of ASF1B in human B-cell proliferation by promoting S-phase entry and mitotic progression [11].…”

Comprehensive Analysis Identified ASF1B as an Independent Prognostic Factor for HBV-Infected Hepatocellular Carcinoma

“…ASF1B was previously identified in human islet β-cell replication, and it significantly increased islet β-cell proliferation ( 29 ). In addition, ASF1B overexpression promotes melanoma cell growth and adhesion and inhibits apoptosis ( 30 ). Furthermore, ASF1B has been shown to promote the proliferation and invasion of clear cell renal cell carcinoma and gastric cancer cells through the activation of the AKT and Bax/Bcl-2-p53 pathways ( 31 , 32 ).…”