GENTAUR Belgium BVBA BE0473327336 Voortstraat 49, 1910 Kampenhout BELGIUM Tel 0032 16 58 90 45
GENTAUR U.S.A Genprice Inc,Logistics 547 Yurok Circle, SanJose, CA 95123
Tel (408) 780-0908, Fax (408) 780-0908, [email protected]

Did you know ? If you order before Friday 14h we deliver 90PCT of the the time next Tuesday, Gentaur another in time delivery

Pubmed ID: 31819003
Publication Date: 2019/12/09

Aberrant activation of hepatocyte growth factor/MET signaling promotes β-catenin-mediated prostatic tumorigenesis.


Co-occurrence of aberrant hepatocyte growth factor (HGF)/MET proto-oncogene receptor tyrosine kinase (MET) and Wnt/β-catenin signaling pathways has been observed in advanced and metastatic prostate cancers. This co-occurrence positively correlates with prostate cancer progression and castration-resistant prostate cancer development. However, the biological consequences of these abnormalities in these disease processes remain largely unknown. Here, we investigated the aberrant activation of HGF/MET and Wnt/β-catenin cascades in prostate tumorigenesis by using a newly generated mouse model in which both murine transgene and stabilized β-catenin are conditionally co-expressed in prostatic epithelial cells. These compound mice displayed accelerated prostate tumor formation and invasion compared with their littermates that expressed only stabilized β-catenin. RNA-Seq and quantitative RT-PCR analyses revealed increased expression of genes associated with tumor cell proliferation, progression, and metastasis. Moreover, Wnt signaling pathways were robustly enriched in prostate tumor samples from the compound mice. ChIP-qPCR experiments revealed increased β-catenin recruitment within the regulatory regions of the gene in tumor cells of the compound mice. Interestingly, the occupancy of MET on the promoter also appeared in the compound mouse tumor samples, implicating a novel role of MET in β-catenin-mediated transcription. Results from implanting prostate graft tissues derived from the compound mice and controls into HGF-transgenic mice further uncovered that HGF induces prostatic oncogenic transformation and cell growth. These results indicate a role of HGF/MET in β-catenin-mediated prostate cancer cell growth and progression and implicate a molecular mechanism whereby nuclear MET promotes aberrant Wnt/β-catenin signaling-mediated prostate tumorigenesis.
Authors: Aldahl Joseph , Mi Jiaqi , Pineda Ariana , Kim Won Kyung , Olson Adam , Hooker Erika , He Yongfeng , Yu Eun-Jeong , Le Vien , Lee Dong-Hoon , Geradts Joseph , Sun Zijie ,

Reference:

  1. ncbi.nlm.nih.gov. [Last access 2019/12/09].

Related products :

Catalog number Product name Quantity
25-948 Hepatocyte growth factor regulates cell growth, cell motility, and morphogenesis by activating a tyrosine kinase signaling cascade after binding to the proto-oncogenic c-Met receptor. Hepatocyte growt 0.05 mg
30-077 ERRs, which are coexpressed with ERs in prostatic cells, could regulate cell growth and modulate ER-mediated pathways via interference on ERalpha transcription in prostatic cells. Not only PNRC2 but a 0.05 mg
27-388 ERRs, which are coexpressed with ERs in prostatic cells, could regulate cell growth and modulate ER-mediated pathways via interference on ERalpha transcription in prostatic cells. Not only PNRC2 but a 0.1 mg
28-795 IRF5 is a member of the interferon regulatory factor (IRF) family, a group of transcription factors with diverse roles, including virus-mediated activation of interferon, and modulation of cell growth 0.1 mg
26-210 LAX1 is a single-pass type III membrane protein. It negatively regulates TCR (T-cell antigen receptor)-mediated signaling in T-cells and BCR (B-cell antigen receptor)-mediated signaling in B-cells. 0.05 mg