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Updated: Jan 13, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Rutin Suppresses EMT and Induces Mitochondrial Biogenesis via ER Stress-linked AMPK/SIRT1 Signaling in Prostate
Sih-Han Chen1,2,3, Richard C Wu1,2,3, Wei-Lun Huang1,2
1Department of Nursing, I-Shou University, Kaohsiung, Taiwan, R.O.C.
Background/Aim:
Prostate cancer is the second most commonly diagnosed malignancy and a leading cause of cancer-related mortality among men worldwide. While early-stage disease can often be managed effectively, advanced and treatment-resistant forms such as castration-resistant prostate cancer (CRPC) remain a major therapeutic challenge. Novel therapeutic strategies targeting alternative pathways are therefore urgently needed. Rutin, a natural flavonoid abundant in fruits and vegetables, has demonstrated antioxidant and anticancer properties. This study aimed to investigate the anticancer effects of Rutin in prostate cancer cells, focusing on epithelial-mesenchymal transition (EMT), mitochondrial biogenesis, and endoplasmic reticulum (ER) stress-linked signaling.
Materials And Methods:
Four prostate cancer cell lines (PC-3, DU-145, LNCaP, and LNCaP-Enz) were treated with rutin. Cell proliferation was assessed, and EMT markers [E-cadherin, α-smooth muscle actin (α-SMA), Snail, Slug], mitochondrial biogenesis-related proteins (AMPK, SIRT1, PGC-1α, NRF1, TFAM), and ER stress markers (BiP, IRE1, PERK, ATF6) were analyzed by standard molecular and cellular assays. Co-treatment with the ER stress inhibitor TUDCA and the eIF2α phosphorylation modulator Salubrinal was performed to determine pathway involvement.
Results:
Rutin significantly suppressed cell proliferation and EMT in all tested prostate cancer cell lines, as indicated by increased E-cadherin expression and decreased α-SMA, Snail, and Slug. It also promoted mitochondrial biogenesis through the up-regulation of AMPK, SIRT1, PGC-1α, NRF1, and TFAM. In parallel, rutin reduced ER stress marker expression, and these effects were reversed by co-treatment with TUDCA or Salubrinal.
Conclusion:
Rutin inhibits prostate cancer progression by suppressing EMT, inducing mitochondrial biogenesis, and acting via ER stress-linked AMPK/SIRT1 signaling. These findings suggest that Rutin may serve as a potential therapeutic candidate for advanced prostate cancer.
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