KLF10 upregulates ACSM3 via the PI3K/Akt signaling pathway to inhibit the malignant progression of melanoma
- Zhirong Zhao
- Yuanchang Zhan
- Li Jing
- Huali Zhai
Affiliations: Department of Clinical Laboratory, Xi'an Dian Medical Laboratory Co., Ltd., Xi'an Shaanxi 210016, P.R. China, Department of Clinical Laboratory, Xi'an Aerospace General Hospital, Xi'an, Shaanxi 710000, P.R. China, Department of Clinical Laboratory Jingbian County People's Hospital, Yulin, Shaanxi 718500, P.R. China, Department of Clinical Laboratory, Changan Hospital, Xi'an, Shaanxi 710000, P.R. China
- Published online on: April 13, 2022 https://doi.org/10.3892/ol.2022.13295
Copyright: © Zhao
et al. This is an open access article distributed under the
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Malignant melanoma is a type of skin cancer caused by mutations in the DNA of melanocytes. Melanoma is relatively rare compared with other types of skin tumors, but has a highly aggressive biological behavior and consequently, a poorer prognosis. Therefore, the present study aimed to explore the role and mechanism of Kruppel‑like factor 10 (KLF10) and acyl‑CoA medium‑chain synthetase 3 (ACSM3) in melanoma progression. KLF10 expression in melanoma tissues was predicted using Gene Expression Profiling Interactive Analysis (GEPIA). KLF10 expression in healthy and melanoma cells was also detected using reverse transcription‑quantitative PCR and western blotting. Cell transfection was performed to overexpress KLF10 or silence ACSM3. Cell viability, proliferation, migration, invasion and apoptosis were detected using Cell Counting Kit‑8, colony formation, wound healing, Transwell and TUNEL assays, respectively. The activity of the ACSM3 promoter was detected using a dual‑luciferase reporter assay, and the relationship between KLF10 and ACSM3 was detected using the GEPIA database and chromatin immunoprecipitation (ChIP). The results demonstrated that KLF10 expression was significantly downregulated in melanoma cells, especially in A375 cells. Compared with the Ov‑NC group, KLF10 overexpression significantly inhibited the proliferation, invasion and migration of melanoma cells and promoted their apoptosis. Similar to KLF10, ACSM3 was also downregulated in A375 cells compared with that in the HEM group, and the GEPIA database analysis and ChIP assay results demonstrated that KLF10 expression was positively associated with ACSM3 expression. Furthermore, silencing ACSM3 significantly reversed the effect of KLF10 overexpression on cell proliferation, invasion and migration, and ACSM3 knockdown increased the levels of phosphorylated (p)‑PI3K and p‑Akt compared with the levels in the Ov‑KLF10 + sh‑NC group. Overall, the present study suggested that KLF10 inhibited the proliferation, invasion and migration of melanoma cells by targeting ACSM3 via the PI3K/Akt signaling pathway.