Melatonin inhibits ESCC tumor growth by mitigating the HDAC7/?-catenin/c-Myc positive feedback loop and suppressing the USP10-maintained HDAC7 protein stability.

Melatonin, a natural hormone secreted by the pineal gland, has been reported to exhibit antitumor properties through diverse mechanisms of action. However, the oncostatic function of melatonin on esophageal squamous cell carcinoma (ESCC) remains elusive. This study was conducted to investigate the potential effect and underlying molecular mechanism of melatonin ...
as single anticancer agent against ESCC cells.ESCC cell lines treated with or without melatonin were used in this study. In vitro colony formation and EdU incorporation assays, and nude mice tumor xenograft model were used to confirm the proliferative capacities of ESCC cells. RNA-seq, qPCR, Western blotting, recombinant lentivirus-mediated target gene overexpression or knockdown, plasmids transfection and co-IP were applied to investigate the underlying molecular mechanism by which melatonin inhibited ESCC cell growth. IHC staining on ESCC tissue microarray and further survival analyses were performed to explore the relationship between target genes' expression and prognosis of ESCC.Melatonin treatment dose-dependently inhibited the proliferative ability and the expression of histone deacetylase 7 (HDAC7), c-Myc and ubiquitin-specific peptidase 10 (USP10) in ESCC cells (P?
Mesh Terms:
Animals, Catenins, Cell Proliferation, Esophageal Neoplasms, Esophageal Squamous Cell Carcinoma, Feedback, Histone Deacetylases, Humans, Melatonin, Mice, Mice, Nude, Protein Stability, Proto-Oncogene Proteins c-myc, Ubiquitin Thiolesterase, Ubiquitin-Specific Proteases, beta Catenin
Mil Med Res
Date: Sep. 27, 2022
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