Open AccessKnockdown of PLCB2 expression reduces melanoma cell viability and promotes melanoma cell apoptosis by altering Ras/Raf/MAPK signals
Author(s) -
Huahui Zhang,
Tao Xie,
Yongjie Shui,
Yiying Qi
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10798
Subject(s) - gene knockdown , viability assay , cell cycle , biology , melanoma , oncogene , cancer research , apoptosis , cell growth , mapk/erk pathway , cell , signal transduction , microbiology and biotechnology , genetics
Malignant melanoma has the highest malignancy rate among all skin cancer and is characterized by an insidious onset, high invasion and poor patient prognosis. Yet, the mechanisms involved remain unclear and warrant further investigation. Based on bioinformatic analysis, phospholipase C β2 (PLCB2) has been found to be correlated with melanoma growth. The present study was the first to demonstrate that PLCB2 is a key factor affecting melanoma proliferation and apoptosis. Here, microarray datasets from the publicly available Gene Expression Omnibus (GEO) database were employed, and gene set enrichment analysis (GSEA) was introduced to identify candidate transcription factors. PLCB2 was identified as a crucial gene in the protein‑protein interaction (PPI) network. The expression of PLCB2 mRNA in various cancer lines was analyzed by reverse transcription‑polymerase chain reaction (RT‑PCR). In addition, the proliferation ability and apoptosis rate in human melanoma cells overexpressing or not overexpressing PLCB2 were assessed using colony formation assay, flow cytometry and the Cell Counting Kit‑8 (CCK‑8) assay. Cell viability and apoptosis‑related factors, such as p53, Bcl‑2, Bax and caspase‑3 were significantly regulated. Knockdown of PLCB2 suppressed the activation of the Ras/Raf/MAPK signaling pathway. In conclusion, knockdown of PLCB2 suppressed cell viability and promoted cell apoptosis by activating the Ras/Raf/MAPK pathway. Thus, PLCB2 may utilized as a potential therapeutic target in patients with melanoma.