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Solamargine inhibits the growth of hepatocellular carcinoma and enhances the anticancer effect of sorafenib by regulating HOTTIP-TUG1/miR-4726-5p/MUC1 pathway. | LitMetric

Solamargine inhibits the growth of hepatocellular carcinoma and enhances the anticancer effect of sorafenib by regulating HOTTIP-TUG1/miR-4726-5p/MUC1 pathway.

Mol Carcinog

Department of Oncology, Clinical and Basic Research Team of TCM Prevention and Treatment of NSCLC, The Second Clinical College of Guangzhou University of Chinese Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong, P.R. China.

Published: April 2022

AI Article Synopsis

  • Hepatocellular carcinoma (HCC) is a prevalent type of liver cancer, and the effectiveness of sorafenib (SF), its main treatment, is often limited by drug resistance.
  • The study found that solamargine (SM), a natural compound, effectively inhibits HCC cell growth and works alongside SF to enhance its anticancer effects.
  • SM's mechanism involves downregulating specific long noncoding RNAs and increasing a certain microRNA, which in turn reduces the levels of the protein MUC1, a crucial player in tumor growth and responsiveness to treatment, suggesting new strategies for HCC therapy.

Article Abstract

Hepatocellular carcinoma (HCC) is one of the most common primary malignancies. Drug resistance has significantly prevented the clinical application of sorafenib (SF), a first-line targeted medicine for the treatment of HCC. Solamargine (SM), a natural alkaloid, has shown potential antitumor activity, but studies about antitumor effect of SM are obviously insufficient in HCC. In the present study, we found that SM significantly inhibited the growth of HCC and enhanced the anticancer effect of SF. In brief, SM significantly inhibited the growth of HepG2 and Huh-7 cells. The combination of SM and SF showed a synergistic antitumor effect. Mechanistically, SM downregulated the expression of long noncoding RNA HOTTIP and TUG1, followed by increasing the expression of miR-4726-5p. Moreover, miR-4726-5p directly bound to the 3'-UTR region of MUC1 and decreased the expression of MUC1 protein. Overexpression of MUC1 partially reversed the inhibitory effect of SM on HepG2 and Huh-7 cells viability, which suggested that MUC1 may be the key target in SM-induced growth inhibition of HCC. More importantly, the combination of SM and SF synergistically restrained the expression of MUC1 protein. Taken together, our study revealed that SM inhibited the growth of HCC and enhanced the anticancer effect of SF through HOTTIP-TUG1/miR-4726-5p/MUC1 signaling pathway. These findings will provide potential therapeutic targets and strategies for the treatment of HCC.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9302658PMC
http://dx.doi.org/10.1002/mc.23389DOI Listing

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