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Up‐regulation of KISS1 as a novel target of Let‐7i in melanoma serves as a potential suppressor of migration and proliferation in vitro
Melanoma is a kind of skin cancer that is begun by the alteration of melanocytes. miRNAs are small non‐coding RNA molecules that regulate a variety of biological processes. KISS1, the metastasis‐suppressor gene, encodes kisspeptins which inhibits migration and proliferation of cancers. This study wa...
Autores principales: | , , , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278109/ https://www.ncbi.nlm.nih.gov/pubmed/34096173 http://dx.doi.org/10.1111/jcmm.16695 |
Sumario: | Melanoma is a kind of skin cancer that is begun by the alteration of melanocytes. miRNAs are small non‐coding RNA molecules that regulate a variety of biological processes. KISS1, the metastasis‐suppressor gene, encodes kisspeptins which inhibits migration and proliferation of cancers. This study was aimed to determine the role of Let‐7i and KISS1 in melanoma cell migration and proliferation. At first, the expression of Let‐7i and KISS1 was determined in patients with melanoma. In the in vitro part of the study, Let‐7i mimics were transfected and the impact of its restoration on target gene expression, proliferation, migration and apoptosis of SK‐MEL‐3 melanoma cell line was assessed by real‐time PCR and Western blotting, MTT assay, wound‐healing assay and flow cytometry, respectively. Besides, KISS1 inhibitor siRNA alone and along with Let‐7i was transfected to determine their probable correlation. The results revealed that either Let‐7i or KISS1 were down‐regulated in patients with melanoma. The results obtained from the in vitro part of the study revealed that restoration of Let‐7i reduced the expression of metastasis‐ and proliferation‐related target genes. Moreover, it was revealed that up‐regulation of Let‐7i attenuated migration and proliferation capability of SK‐MEL‐3 cells. Besides, it was demonstrated that Let‐7i restoration induced apoptosis in melanoma cells. More importantly, the KISS1 inhibitor caused a prominent cell migration and proliferation, attenuated by Let‐7i re‐expression. To sum up, the present study revealed the impressive role of Let‐7i restoration along with its correlation with KISS1 on melanoma carcinogenicity which may be applicable in future in vivo studies. |
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