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dc.contributor.authorWang, Shumei-
dc.contributor.authorQiu, Liyun-
dc.contributor.authorSong, Haiyan-
dc.contributor.authorDang, Ningning-
dc.date.accessioned2019-11-05T12:51:50Z
dc.date.available2019-11-05T12:51:50Z
dc.date.issued2018
dc.identifier.citationWang, Shumei ; Qiu, Liyun ; Song, Haiyan ; Dang, Ningning ; NPS - 2143 (hydrochloride) inhibits melanoma cancer cell proliferation and induces autophagy and apoptosis, Med Sci (Paris), , Vol. 34, N° HS ; p. 87-93 ; DOI : 10.1051/medsci/201834f115
dc.identifier.issn1958-5381
dc.identifier.urihttp://hdl.handle.net/10608/9992
dc.description.abstractMelanoma is a common and aggressive skin cancer caused by the oncogenic transformation of melanocytes. NPS-2143 (hydrochloride) is a calcification drug that acts as an antagonist of the calcium-sensing receptor (CaSR) and consequently stimulates the release of parathyroid hormone. In the present work, we treated cells from the human melanoma cell line M14 to investigate the effects of NPS-2143 on melanoma cells and elucidate their underlying mechanisms. We observed that NPS-2143 inhibits the survival and proliferation of M14 cells and suppresses the migration and proliferation of M14 cells by inducing apoptosis. The Bax/Bcl‑2 ratio in M14 cells was enhanced by the NPS-2143 treatment, suggesting that the mitochondrial apoptotic pathway was activated. The expression and phosphorylation of proteins involved in the PI3K signaling pathway were altered by NPS-2143 treatment. Our data show that NPS-2143 impacts the viability and induces the apoptosis of melanoma M14 cells through its impact on the PI3K signaling pathway. It suggests that NPS-2143 could represent a promising candidate for melanoma treatment.en
dc.language.isoen
dc.publisherEDP Sciences
dc.rightsArticle en libre accèsfr
dc.rightsMédecine/Sciences - Inserm - SRMSfr
dc.sourceM/S. Médecine sciences [ISSN papier : 0767-0974 ; ISSN numérique : 1958-5381], , Vol. 34, N° HS; p. 87-93
dc.titleNPS - 2143 (hydrochloride) inhibits melanoma cancer cell proliferation and induces autophagy and apoptosisen
dc.typeArticle
dc.contributor.affiliationDepartment of Community Medicine, Jinan Central Hospital affiliated to Shandong University, No.105 Jiefang Road, Jinan 250013, Shandong Province, China
dc.contributor.affiliationDepartment of Pharmacy, Jinan Central Hospital affiliated to Shandong University, No.105 Jiefang Road, Jinan 250013, Shandong Province, China
dc.contributor.affiliationDepartment of Dermatology, Jinan Central Hospital affiliated to Shandong University, No.105 Jiefang Road, Jinan 250013, Shandong Province, China
dc.identifier.doi10.1051/medsci/201834f115


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