miR-596 Modulates Melanoma Growth by Regulating Cell Survival and Death

Liu, Szumam; Lin, Chen; Lu, Jean; Lin, In Yu; Tsai, Mu Shiun; Chen, Ming Hong; Ma, Nianhan

doi:10.1016/j.jid.2017.11.016

Cited by 23 publications

(14 citation statements)

References 35 publications

(48 reference statements)

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“…Consistently, we also proved the down-regulation of miR-596 in EOC cells. More importantly, our work detected From these findings, we firstly identified miR-596 as a novel tumor-inhibitor in EOC, which was similar to several previous reports regarding miR-596 function in malignancies including melanoma [14], oral cancer [25] and gastric cancer [13].…”

Section: Discussionsupporting

confidence: 88%

“…For examples, circRNA AGFG1 acts as a sponge of miR-195-5p to promote triple-negative breast cancer progression through regulating CCNE1 expression [10]; miR-760 suppresses human colorectal cancer cell growth by targeting BATF3AP-1/ cyclinD1 signaling [11]; MiR-4319 suppresses the malignancy of triple-negative breast cancer by regulating self-renewal of cancer stem cells [12]. Recently, several researches have demonstrated the tumor suppressive role of miR-596 in malignancies such as gastric cancer [13] and melanoma [14]. Besides, a former report revealed that miR-596 is expressed at a low level in EOC [15].…”

Section: Introductionmentioning

confidence: 99%

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MiR-596 activated by EP300 controls the tumorigenesis in epithelial ovarian cancer by declining BRD4 and KPNA4

Wang

Cui

et al. 2020

Cancer Cell Int

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Background Epithelial ovarian cancer (EOC), a subclass of ovarian cancer (OC), is usually diagnosed at advanced stages due to the lack of effective screening means. Mounting reports have disclosed the vitally important roles of microRNAs (miRNAs) in carcinogenesis. Here, we aimed to find out possible miRNAs participating in EOC development. Methods qRT-PCR ad western blot respectively examined the mRNA and protein levels of studied genes. CCK-8, colony formation, flow cytometry, TUNEL and spheroid formation assays were appropriately employed for examining cell proliferation, cell cycle, apoptosis and stemness. The interaction between molecules was affirmed by luciferase reporter, RNA pull down and ChIP assays. Results In consistent with the observation of a past study, miR-596 expression was relatively low in EOC cells. Up-regulating miR-596 suppressed EOC cell proliferation and stemness. EP300 transcriptionally activated miR-596 to serve as a tumor-repressor in EOC. Then BRD4 and KPNA4, whose knockdown led to restraining effects on cell growth and stemness, were both revealed to be targeted by miR-596 in EOC. Lastly, rescue assays affirmed the tumor-restraining role of miR-596-BRD4/KPNA4 axis in EOC. Conclusion EP300-activated miR-596 hampered cell growth and stemness via targeting BRD4 and KPNA4 in EOC, proofing miR-596 as a promising therapeutic target in treating EOC patients.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

MiR-596 activated by EP300 controls the tumorigenesis in epithelial ovarian cancer by declining BRD4 and KPNA4

Wang

Cui

et al. 2020

Cancer Cell Int

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“…As a miRNA located on human chromosome 8p23.3, miR-596 acts as an antioncogene in a variety of tumors [44]. Endo et al demonstrated that miR-596 inhibited the growth of oral cancer through targeting LGALS3BP [45].…”

Section: Discussionmentioning

confidence: 99%

MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head

Liu

Lei

2020

J Orthop Surg Res

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Background: It is reported that miR-596 has a potential diagnostic value for non-traumatic osteonecrosis of the femoral head (NOFH), but its underlying mechanisms in NOFH is unclear. Methods: The expression of miR-596 and Smad3 was detected by western blot and quantitative real-time PCR. The relationship between the two molecules was explored using Dual-Luciferase Reporter Assay. Glucocorticoid (GC)dexamethasone, was used to induce bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation, and the effects of miR-596 on BMSC osteogenic differentiation and proliferation were determined.Results: MiR-596 expression was upregulated, while Smad3 expression was inhibited in the bone marrow samples of patients with steroid-induced osteonecrosis of femoral head (SANFH). Overexpression of miR-596 inhibited the proliferation and osteogenic differentiation of BMSCs induced by GC. Meanwhile, the opposite results were observed in the miR-596 inhibitor group. In addition, Smad3 was a target gene of miR-596, and negatively regulated by miR-596. The promotion effect of the miR-596 inhibitor on BMSC proliferation and osteogenic differentiation was reversed by si-Smad3.Conclusion: MiR-596 can suppress GC-BMSC osteoblastic differentiation and proliferation by regulating Smad3 expression.

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“…To date, vemurafenib, ipilimumab, sibutramine and other targeted drugs have been recommended for the treatment of malignant melanoma. However, malignant melanoma is not completely cured by these agents (12). Metastasis may occur during the early stages of cutaneous malignant melanoma and prognosis is often poor.…”

Section: Introductionmentioning

confidence: 99%

Bufotalin induces cell cycle arrest and cell apoptosis in human malignant melanoma A375 cells

Pan

Chen

et al. 2019

Oncol Rep

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Venenum bufonis has been used as an antitumor drug in China for many years. Bufotalin, as an active component of Venenum bufonis, has been proven to exhibit antitumor effects in cancer types. In the present study, the effect of bufotalin on the human melanoma skin cancer cell line A375 was analyzed using MTT and colony formation assays. Bufotalin significantly inhibited the proliferation and colony formation of A375 cells. Further studies demonstrated that bufotalin significantly upregulated the protein levels of ATM serine/threonine kinase and Chk2, downregulated CDC25C protein expression, and subsequently inhibited CDK1 expression, leading to cell cycle arrest at the G2/M phase of the A375 cells. Furthermore, bufotalin significantly increased BAX expression levels, decreased BCL-2 expression, and then upregulated apoptosis-related proteins, caspase-3/-9, followed by A375 cell apoptosis. Taken together, these results show that bufotalin induces cell cycle arrest at the G2/M phase and cell apoptosis, resulting in the inhibition of A375 cell proliferation, thereby suggesting that bufotalin may be utilized in melanoma treatment.

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miR-596 Modulates Melanoma Growth by Regulating Cell Survival and Death

Cited by 23 publications

References 35 publications

MiR-596 activated by EP300 controls the tumorigenesis in epithelial ovarian cancer by declining BRD4 and KPNA4

MiR-596 activated by EP300 controls the tumorigenesis in epithelial ovarian cancer by declining BRD4 and KPNA4

MiR-596 inhibits osteoblastic differentiation and cell proliferation by targeting Smad3 in steroid-induced osteonecrosis of femoral head

Bufotalin induces cell cycle arrest and cell apoptosis in human malignant melanoma A375 cells

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