ArticleCancer science2021
Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis.
Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Nectin-4 expression in upper and lower tract urothelial carcinoma: correlation with early-stage disease and prognostic relevance.Virchows Archiv : an international journal of pathology · 2026Article
- Polarity protein Par3 deficiency promotes metastasis of bladder cancer via interaction of Ppp1r12c.Biology direct · 2026Article
- The polarity protein Par3 enhances renal cell carcinoma metastasisCancer biology & medicine · 2025Article
- Capn4 regulates Snail to promote the epithelial-mesenchymal transition of nasopharyngeal carcinoma by mediating the transcriptional activity of claudin-11.The Kaohsiung journal of medical sciences · 2023Article
- Role of Cell-Cell Junctions in Oesophageal Squamous Cell Carcinoma.Biomolecules · 2022Review
- Establishment of an optimized orthotopic bladder cancer model in mice.BMC urology · 2022Article
- Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest.Breast cancer research and treatment · 2022Article
- miR-559 Inhibits Proliferation, Autophagy, and Angiogenesis of Hepatocellular Carcinoma Cells by Targeting PARD3.Mediators of inflammation · 2022Article
- Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis.Cancer science · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Bladder cancer (BLCA) remains the leading cause of cancer-related mortality among genitourinary malignancies worldwide. BLCA metastasis represents the primary reason for its poor prognosis. In this study, we report that decreased expression of partitioning defective 3 (Par3), a polarity protein (encoded by PARD3), is associated with tumor aggressive phenotypes and poor prognosis in BLCA patients. Consistently, ablation of Par3 promotes the metastasis and invasion of BLCA cells in vitro and in vivo. Further studies reveal that zinc finger protein Snail represses the expression of Par3 by binding to E2-box (CAGGTG) of PARD3 promoter-proximal. Inhibition of GSK-3β promotes the expression and nuclear localization of Snail and then reduces the expression of Par3, resulting in the metastasis and invasion of BLCA cells. Moreover, we detected the interaction between Par3 (936-1356 aa) and ZO-1 (1372-1748 aa), which is involved in the maintenance of tight junction. Together, our results demonstrate that the GSK-3β/Snail/Par3/ZO-1 axis regulates BLCA metastasis, and Snail is a major regulator for Par3 protein expression in BLCA.
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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 Socratic graph.