AI Article Synopsis

  • This study examines the effects of swertiamarin on hepatocellular carcinoma (HCC) cells, focusing on its impact on cell viability, apoptosis, and invasion in HepG2 cells, and tumor growth in SK-Hep-1 xenografts in mice.
  • Results indicate that swertiamarin decreases cell viability and invasion while increasing apoptosis in HepG2 cells, and significantly inhibits tumor growth in the mouse model.
  • Bioinformatics analysis of gene expression changes revealed that swertiamarin primarily affects the PI3k-Akt pathway and identified multiple significant gene targets, including JUN and STAT3, which could help understand its anti-tumor mechanisms for potential cancer treatment.

Article Abstract

: To explore gene expression profiling in hepatocellular carcinoma (HCC) cells exposed to swertiamarin. : Cell viability, apoptosis and invasion were examined in HepG2 cells after swertiamarin treatment. Tumor growth of SK-Hep-1 cells xenografted in nude mice was monitored after swertiamarin treatment. Total RNA was isolated from HepG2 cells treated with swertiamarin for microarray analysis. The data of microarray were analyzed by bioinformatics. : Swertiamarin treatment decreased the viability and invasion while increased the apoptosis of HepG2 cells, and significantly inhibited the growth of SK-Hep-1 cells xenografted in nude mice. Pathway and biological process analysis of differentially expressed genes (DEGs) in swertiamarin treated HepG2 cells showed that PI3k-Akt was the most significant regulated pathway. 47 targets of swertiamarin were predicted by CGBVS while 21 targets were predicted by 3NN. Notably, 8 targets were predicted as the targets of swertiamarin by both programs, including two prominent targets JUN and STAT3. A large range of DEGs induced by swertiamarin could be regulated by JUN and STAT3. : Swertiamarin treatment led to significant changes in the expression of a variety of genes that modulate cell survival, cell cycle progression, apoptosis, and invasion. Moreover, most of these genes can be clustered into pathway networks such as PI3K, JUN, STAT3, which are predicted targets of swertiamarin. Further confirmation of these targets will reveal the anti-tumor mechanisms of swertiamarin and facilitate the development of swertiamarin as a novel agent for cancer prevention and treatment.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6856900PMC
http://dx.doi.org/10.7150/jca.33666DOI Listing

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