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Flavonoids Luteolin and Quercetin Inhibit RPS19 and contributes to metastasis of cancer cells through c-Myc reduction

Ku-Chung Chen1,2, Wen-Hsien Hsu1,3, Jhih-Yun Ho2

  • 1Department of Biochemistry and Molecular Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Journal of Food and Drug Analysis
|July 7, 2018
PubMed

Insights

Flavonoids luteolin and quercetin inhibit cancer cell metastasis by targeting RPS19. They block the Akt/mTOR/c-Myc pathway, suppressing RPS19-activated epithelial-mesenchymal transition (EMT) signaling.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Flavonoids luteolin and quercetin are known to inhibit cancer cell growth and metastasis.
  • Previous studies demonstrated their ability to block the Akt/mTOR/c-Myc signaling pathway.

Purpose of the Study:

  • To investigate the inhibitory mechanism of luteolin and quercetin on RPS19 expression and activity in cancer cells.
  • To elucidate the role of RPS19 in cancer cell metastasis and its regulation by the Akt/mTOR/c-Myc pathway.

Main Methods:

  • Investigated the effect of luteolin and quercetin on RPS19 protein levels and transactivation activity in A431-III cells.
  • Analyzed c-Myc binding sites on the RPS19 promoter.
  • Utilized specific inhibitors (LY294002, rapamycin, 10058-F4) and genetic manipulation (overexpression, knockdown) of c-Myc and RPS19.
  • Assessed epithelial-mesenchymal transition (EMT) markers and cancer cell metastasis abilities.

Main Results:

  • Luteolin and quercetin reduced RPS19 protein level and transactivation activity in A431-III cells.
  • c-Myc was identified to bind to the RPS19 promoter, regulating its expression and activity.
  • Inhibitors of Akt, mTOR, and c-Myc, as well as c-Myc manipulation, significantly affected RPS19 expression.
  • RPS19 was found to regulate EMT markers and cancer cell metastasis.

Conclusions:

  • Luteolin and quercetin inhibit cancer cell metastasis by suppressing RPS19.
  • The mechanism involves blocking the Akt/mTOR/c-Myc signaling pathway, which in turn suppresses RPS19-activated EMT signaling.
Keywords:
EMTLuteolinQuercetinRPS19c-Myc

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