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ATP-P2Y2-β-catenin axis promotes cell invasion in breast cancer cells.

ABSTRACT: Extracellular adenosine 5'-triphosphate (ATP), secreted by living cancer cells or released by necrotic tumor cells, plays an important role in tumor invasion and metastasis. Our previous study demonstrated that ATP treatment in vitro could promote invasion in human prostate cancer cells via P2Y2, a preferred receptor for ATP, by enhancing EMT process. However, the pro-invasion mechanisms of ATP and P2Y2 are still poorly studied in breast cancer. In this study, we found that P2Y2 was highly expressed in breast cancer cells and associated with human breast cancer metastasis. ATP could promote the in vitro invasion of breast cancer cells and enhance the expression of β-catenin as well as its downstream target genes CD44, c-Myc and cyclin D1, while P2Y2 knockdown attenuated above ATP-driven events in vitro and in vivo. Furthermore, iCRT14, a β-catenin/TCF complex inhibitor, could also suppress ATP-driven migration and invasion in vitro. These results suggest that ATP promoted breast cancer cell invasion via P2Y2-β-catenin axis. Thus blockade of the ATP-P2Y2-β-catenin axis could suppress the invasive and metastatic potential of breast cancer cells and may serve as potential targets for therapeutic interventions of breast cancer.

SUBMITTER: Zhang JL

PROVIDER: S-EPMC5497932 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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ATP-P2Y2-β-catenin axis promotes cell invasion in breast cancer cells.

Zhang Jiang-Lan JL Liu Ying Y Yang Hui H Zhang Hong-Quan HQ Tian Xin-Xia XX Fang Wei-Gang WG

Cancer science 20170606 7

Extracellular adenosine 5'-triphosphate (ATP), secreted by living cancer cells or released by necrotic tumor cells, plays an important role in tumor invasion and metastasis. Our previous study demonstrated that ATP treatment in vitro could promote invasion in human prostate cancer cells via P2Y2, a preferred receptor for ATP, by enhancing EMT process. However, the pro-invasion mechanisms of ATP and P2Y2 are still poorly studied in breast cancer. In this study, we found that P2Y2 was highly expre ...[more]

PMID: 28474758

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Project description:BackgroundAlthough Cell growth regulator with EF-hand domain 1 (CGREF1) has been predicted to be upregulated in multiple cancer types, its definitive function role in carcinogenesis, particularly in hepatocellular carcinoma (HCC), remains poorly characterized.MethodsComprehensive bioinformatics analysis was initially conducted using the University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) and Gene Expression Profiling Interactive Analysis (GEPIA) databases to investigate CGREF1 mRNA expression patterns in HCC tissues and their clinical correlation with patient survival outcomes. Experimental validation was subsequently performed through real-time quantitative polymerase chain reaction (RT-qPCR), immunohistochemistry (IHC), and Western blot techniques. Functional characterization studies employing genetic knockdown and overexpression models in HCC cell lines demonstrated CGREF1's regulatory effects on malignant phenotypes, as evidenced by 3-(4,5-dimethylthiazolyl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay and Transwell migration and invasion assays. were adopted to investigate the role of CGREF1 in the proliferation, invasion, and migration of HCC cells. Mechanistic investigations integrating bioinformatics predictions with Western blot analysis revealed CGREF1 mediated-modulation of the Wnt/β-Catenin signaling axis, elucidating its molecular underpinnings in HCC progression.ResultsThe results demonstrated that CGREF1 is highly expressed in HCC tissues, and HCC patients with elevated CGREF1 expression exhibited significantly shorter survival times. Upregulation of CGREF1 promoted the proliferation, migration, and invasion of HCC cells, whereas inhibition of CGREF1 expression suppressed these phenotypes. Mechanistically, CGREF1 activates the Wnt/β-Catenin signaling pathway through the upregulation of eukaryotic translation initiation factor 3 H subunit (EIF3H). Furthermore, partial inhibition of EIF3H attenuated the effects of CGREF1 overexpression on the proliferation, migration, and invasion of HCC cells.ConclusionCGREF1 is upregulated in HCC and acted as an oncogene through the CGREF1/EIF3H/Wnt/β-Catenin signaling axis. These findings suggest that CGREF1 may emerge as a potential therapeutic target for HCC.

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ATP-P2Y2-β-catenin axis promotes cell invasion in breast cancer cells.

Publications

ATP-P2Y2-β-catenin axis promotes cell invasion in breast cancer cells.

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