ORIGINAL ARTICLE Quercetin modulates Wnt signaling components in prostate cancer cell line by inhibiting cell viability, migration, and metastases Meghna M. Baruah 1 & Anand P. Khandwekar 1 & Neeti Sharma 1 Received: 27 April 2016 /Accepted: 15 July 2016 # International Society of Oncology and BioMarkers (ISOBM) 2016 Abstract Epithelial-mesenchymal transition (EMT) is a plas- tic transition in tumor progression during which cancer cells undergo dramatic changes acquiring highly invasive proper- ties. Transforming growth factor-β (TGF-β) is an inducer of EMT in epithelial cells and is obligatory for acquiring invasive phenotype in carcinoma. TGF-β plays a vital role in metasta- sis and tumorigenesis in prostate cancer, and mutations in the components of Wnt signaling pathways are associated with various kinds of cancers including prostate cancer. The pur- pose of this study was to identify alterations in Wnt signaling pathway components involved during prostate cancer progres- sion and to determine the effect of quercetin on TGF-β- induced EMT in prostate cancer (PC-3) cell line. The expres- sion of epithelial and mesenchymal markers and the compo- nents of Wnt signaling pathway were evaluated by real-time polymerase chain reaction. It was observed that quercetin prevented TGF-β-induced expression of vimentin and N- cadherin and increased the expression of E-cadherin in PC-3 cells, thus preventing TGF-β-induced EMT. Furthermore, the relative expression of Twist, Snail, and Slug showed that quer- cetin significantly decreased TGF-β-induced expression of Twist, Snail, and Slug. In the present study, the expression of epithelial markers were found to be upregulated in naive state and downregulated in induced state whereas the mesenchymal markers were found to be downregulated in naive state and upregulated in induced state. Thus, our study concludes that quercetin may prevent prostate cancer metas- tasis by regulating the components of Wnt pathway. Keywords EMT . TGF-β . Wnt . quercetin . N-cadherin . E-cadherin Introduction Prostate cancer (PCa) remains one of the major medical bur- dens in males. The estimated number of new cases and deaths from PCa in USA in 2015 are 220,800 and 27,540, respec- tively [1]. The mortality rate of metastatic prostate cancer is even higher despite the chemotherapies. Thus, there is an ur- gent need for therapies for the malignant forms of cancer. Cancer cells undergo dynamic changes to acquire invasive phenotype, and epithelial-mesenchymal transition (EMT) plays an important role in the metastasis of tumors of epithelial origin [2]. It is a developmental program where there is down- regulation of epithelial characteristics and upregulation of mesenchymal phenotypes. Loss of E-cadherin is associated with PCa progression and Gleason grade [3], indicating EMT to be a potent player of PCa metastasis. EMT is involved in the formation of many tissues and organs during develop- ment [4]. Transforming growth factor-β (TGF-β) is an induc- er of EMT in epithelial cells and is obligatory for acquiring invasive phenotype in carcinoma [5, 6]. TGF-β acts as a po- tent inhibitor of epithelial cell proliferation, whereas in con- texts with cancer progression, TGF-β promotes tumor cell survival through autocrine/paracrine interactions within tumor microenvironment. TGF-β also enhances tumor cell prolifer- ation and simultaneously inhibits tumoricidal activity of the immune system, thus accelerating tumor progression [7]. Meghna M. Baruah and Neeti Sharma combined first author. Electronic supplementary material The online version of this article (doi:10.1007/s13277-016-5277-6) contains supplementary material, which is available to authorized users. * Neeti Sharma neetimohan27@gmail.com 1 Symbiosis School of Biomedical Sciences, Symbiosis International University, Gram - Lavale; Taluka - Mulshi, Pune 412115, India Tumor Biol. DOI 10.1007/s13277-016-5277-6