ArticleCancer genomics & proteomics
Rutin Suppresses EMT and Induces Mitochondrial Biogenesis
Article in Cancer genomics & proteomics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- AMPK/ SIRT1 signaling pathway activation acts on PGC-1α/ PPARγ to alleviate sepsis-acquired weakness.Cell death discovery · 2026Article
- Molecular Effects ofInternational journal of molecular sciences · 2026Article
- Article
- NRF1 Activates the AMPK/SIRT1/PGC-1α/TFAM Axis to Suppress EMT and Tumor Progression in Lung Adenocarcinoma.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimProstate 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
methodsFour 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.
resultsRutin 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.
conclusionRutin inhibits prostate cancer progression by suppressing EMT, inducing mitochondrial biogenesis, and acting
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.