Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Centrosomal protein55 enhances melanoma cell proliferation, invasion and migration through PI3K/AKT signaling

Huaikang Hua^1,2, Huifang Yang³

¹Graduate School, Zhejiang Chinese Medical University, Hangzhou, Zhejiang Province 310000, China; ²Department of Cosmetic and Plastic Burn Wound Repair, Lishui People's Hospital, Lishui, Zhejiang Province 323000, China; ³Department of Dermatology, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi Province 341000, China.

For correspondence:- Huifang Yang Email: hfyang3365@163.com Tel:+867978266037

Accepted: 29 September 2022 Published: 28 October 2022

Citation: Hua H, Yang H. Centrosomal protein55 enhances melanoma cell proliferation, invasion and migration through PI3K/AKT signaling. Trop J Pharm Res 2022; 21(10):2065-2070 doi: 10.4314/tjpr.v21i10.4

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the role of centrosomal protein55 (CEP55) in melanoma.

Methods: The CEP55 expression in human melanoma cells and normal human melanocytes were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot. Cell proliferation was evaluated by colony formation and CCK8 assays, while cell cycle was assessed by flow cytometry. Transwell assay was used to investigate cell migration and invasion.

Results: The CEP55 protein expression was higher in A-2058 and A375 melanoma cells than in normal HEMn-LP cells. Overexpression of CEP55 increased melanoma cell viability and the number of melanoma cell colonies (p < 0.01), while CEP55 silencing reduced melanoma cell viability and proliferation. Overexpression of CEP55 promoted cell cycle (p < 0.01) via decreased p21 expression, but increased CyclinD1 and CDK1 expression. Knockdown of CEP55 enhanced p21 expression and reduced CyclinD1 and CDK1 expression to induce cell cycle arrest. Knockdown of CEP55 suppressed melanoma cell migration and invasion by downregulating p-AKT and p-PI3K.

Conclusion: Centrosomal protein55 functions as an oncogene in melanoma by activating PI3K/AKT signaling. Therefore, CEP55 might be a promising target for melanoma diagnosis and treatment.

Keywords: Centrosomal protein55, Melanoma, Proliferation, Migration, Invasion, Cycle, PI3K/AKT