Phellinus gilvus-derived protocatechualdehyde induces G0/G1 phase arrest and apoptosis in murine B16-F10 cells.

Publication date: Mar 01, 2020

Protocatechualdehyde (PCA) is considered to be the main phenolic component of Phellinus gilvus responsible for its anticancer properties. Previous studies have demonstrated that PCA can have an anticancer effect on multiple cancer types, but little is known about the effect of PCA on melanoma cells. The present study investigated the inhibitory abilities and potential anticancer mechanisms of PCA on B16-F10 cells using MTT assay. Cell apoptosis and cell cycle were assessed by flow cytometry using Annexin V-FITC and propidium iodide staining. Whole-transcriptome analysis was used to investigate the effects of PCA on gene expression. PCA significantly decreased cell viability, induced cell cycle arrest at G0/G1 phase and promoted apoptosis of B16-F10 cells, suggesting that PCA could have anticancer effects against melanoma cells. Whole-transcriptome analysis indicated that PCA treatment upregulated genes involved in histone modification and decreased the transcription of genes involved in DNA repair and replication. Kyoto Encyclopedia of Genes and Genomes analysis showed that PCA treatment enhanced the complement and coagulation cascades, and the p53 signaling pathway. The present results indicated that PCA could act as an antitumor agent in melanoma cells, which may provide experimental support for the development of novel therapies to treat melanoma.

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Zhong, S., Jin, Q., Yu, T., Zhu, J., and Li, Y. Phellinus gilvus-derived protocatechualdehyde induces G0/G1 phase arrest and apoptosis in murine B16-F10 cells. 25968. 2020 Mol Med Rep (21):3.

Concepts Keywords
Antitumor Agent Programmed cell death
Apoptosis Melanoma
Coagulation Apoptosis
Complement Immunology
Flow Cytometry Cell signaling
G0 Apoptosis
Histone Modification Cancer
Induced Cycle Medicine
Kyoto Experimental therapies
Melanoma Branches of biology
Murine PCA anticancer melanoma
P53
Phenolic
Staining
Transcription
Transcriptome

Semantics

Type Source Name
drug DRUGBANK Protocatechualdehyde
pathway KEGG Apoptosis
drug DRUGBANK Pidolic Acid
disease MESH cancer
disease MESH melanoma
pathway KEGG Melanoma
pathway KEGG Cell cycle
pathway KEGG Complement and coagulation cascades
pathway KEGG p53 signaling pathway
disease MESH development

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