ArticleOncogene2012
Tumor suppressor Alpha B-crystallin (CRYAB) associates with the cadherin/catenin adherens junction and impairs NPC progression-associated properties.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 71 citations in OpenAlex.
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- Splicing factor derived circular RNA circCAMSAP1 accelerates nasopharyngeal carcinoma tumorigenesis via a SERPINH1/c-Myc positive feedback loop.Molecular cancer · 2022Article
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- Association of Alpha B-Crystallin Expression with Tumor Differentiation Grade in Colorectal Cancer Patients.Diagnostics (Basel, Switzerland) · 2021Article
- Machine learning-based investigation of the cancer protein secretory pathway.PLoS computational biology · 2021Article
- Epigenetic inactivation of IRX4 is responsible for acceleration of cell growth in human pancreatic cancer.Cancer science · 2020Article
- Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma.BMC cancer · 2020Article
- Prognostic value of biomarkers EpCAM and αB-crystallin associated with lymphatic metastasis in breast cancer by iTRAQ analysis.BMC cancer · 2019Article
- Progression of the role of CRYAB in signaling pathways and cancers.OncoTargets and therapy · 2019Review
- Integrative analysis of transcriptomics and clinical data uncovers the tumor-suppressive activity of MITF in prostate cancer.Cell death & disease · 2018Article
- Comprehensive transcriptomic analysis of heat shock proteins in the molecular subtypes of human breast cancer.BMC cancer · 2018Article
- A new long noncoding RNA (lncRNA) is induced in cutaneous squamous cell carcinoma and down-regulates several anticancer and cell differentiation genes in mouse.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpha B-crystallin (CRYAB) maps within the nasopharyngeal carcinoma (NPC) tumor-suppressive critical region 11q22-23 and its downregulation is significantly associated with the progression of NPC. However, little is known about the functional impact of CRYAB on NPC progression. In this study we evaluated the NPC tumor-suppressive and progression-associated functions of CRYAB. Activation of CRYAB suppressed NPC tumor formation in nude mice. Overexpression of CRYAB affected NPC progression-associated phenotypes such as loss of cell adhesion, invasion, interaction with the tumor microenvironment, invasive protrusion formation in three dimensional Matrigel culture, as well as expression of epithelial-mesenchymal transition-associated markers. CRYAB mediates this ability to suppress cancer progression by inhibition of E-cadherin cytoplasmic internalization and maintenance of β-catenin in the membrane that subsequently reduces the levels of expression of critical downstream targets such as cyclin-D1 and c-myc. Both ectopically expressed and recombinant CRYAB proteins were associated with endogenous E-cadherin and β-catenin, and, thus, the cadherin/catenin adherens junction. The CRYAB α-crystallin core domain is responsible for the interaction of CRYAB with both E-cadherin and β-catenin. Taken together, these results indicate that CRYAB functions to suppress NPC progression by associating with the cadherin/catenin adherens junction and modulating the β-catenin function.
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