Psilostachyin C reduces malignant properties of hepatocellular carcinoma cells by blocking CREBBP-mediated transcription of GATAD2B.

Funct Integr Genomics

Department of Neurology, Honghui Hospital, Xi'an Jiaotong University, No. 555, Youyi East Road, Beilin District, Xi'an, Shaanxi, 710054, P.R. China.

Published: April 2024

AI Article Synopsis

  • Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths, prompting research into herbal medicines with anti-tumor effects.
  • Psilostachyin C (PSC), extracted from Artemisia vulgaris L., significantly inhibits the growth, migration, and invasion of HCC cells, while also promoting apoptosis.
  • The study identifies CREBBP as a key target of PSC, as PSC reduces the expression of CREBBP and its downstream target GATAD2B, which is linked to the malignant behaviors of HCC cells.

Article Abstract

Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality globally. Many herbal medicines and their bioactive compounds have shown anti-tumor properties. This study was conducted to examine the effect of psilostachyin C (PSC), a sesquiterpenoid lactone isolated from Artemisia vulgaris L., in the malignant properties of HCC cells. CCK-8, flow cytometry, wound healing, and Transwell assays revealed that 25 μM PSC treatment significantly suppressed proliferation, cell cycle progression, migration, and invasion of two HCC cell lines (Hep 3B and Huh7) while promoting cell apoptosis. Bioinformatics prediction suggests CREB binding protein (CREBBP) as a promising target of PSC. CREBBP activated transcription of GATA zinc finger domain containing 2B (GATAD2B) by binding to its promoter. CREBBP and GATAD2B were highly expressed in clinical HCC tissues and the acquired HCC cell lines, but their expression was reduced by PSC. Either upregulation of CREBBP or GATAD2B restored the malignant properties of HCC cells blocked by PSC. Collectively, this evidence demonstrates that PSC pocessess anti-tumor functions in HCC cells by blocking CREBBP-mediated transcription of GATAD2B.

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Source
http://dx.doi.org/10.1007/s10142-024-01353-8DOI Listing

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