ArticleThe Journal of biological chemistry2011
Structural analysis of the cancer-specific promoter in mesothelin and in other genes overexpressed in cancers.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Decoding the role of mesothelin in tumor dynamics and targeted treatment innovations.Molecular biomedicine · 2025Review
- Multi-Functional Regulation by YAP/TAZ Signaling Networks in Tumor Progression and Metastasis.Cancers · 2023Review
- Review
- A review: hippo signaling pathway promotes tumor invasion and metastasis by regulating target gene expression.Journal of cancer research and clinical oncology · 2021Review
- Free CA125 promotes ovarian cancer cell migration and tumor metastasis by binding Mesothelin to reduce DKK1 expression and activate the SGK3/FOXO3 pathway.International journal of biological sciences · 2021Article
- From Malignant Progression to Therapeutic Targeting: Current Insights of Mesothelin in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2020Review
- YAP1 is an independent prognostic marker in pancreatic cancer and associated with extracellular matrix remodeling.Journal of translational medicine · 2020Article
- Review
- The Role of Mesothelin as a Diagnostic and Therapeutic Target in Pancreatic Ductal Adenocarcinoma: A Comprehensive Review.Targeted oncology · 2018Review
- Article
- Mesothelin Immunotherapy for Cancer: Ready for Prime Time?Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016Review
- Mesothelin as a target for chimeric antigen receptor-modified T cells as anticancer therapy.Immunotherapy · 2016Review
- Serum IGFBP2 and MSLN as diagnostic and prognostic biomarkers for pancreatic cancer.HPB : the official journal of the International Hepato Pancreato Biliary Association · 2014Article
- Discovery of mesothelin and exploiting it as a target for immunotherapy.Cancer research · 2014Review
- Hippo/YAP pathway for targeted therapy.Translational lung cancer research · 2014Review
- C-ERC/mesothelin provokes lymphatic invasion of colorectal adenocarcinoma.Journal of gastroenterology · 2014Article
- "Selective cell death mediated by small conditional RNAs" is not selective.Cancer biology & therapy · 2013Article
- The role of mesothelin in tumor progression and targeted therapy.Anti-cancer agents in medicinal chemistry · 2013Review
- Unbiased discovery of interactions at a control locus driving expression of the cancer-specific therapeutic and diagnostic target, mesothelin.Journal of proteome research · 2012Article
- A thymidylate synthase ternary complex-specific antibody, FTS, permits functional monitoring of fluoropyrimidines dosing.Oncotarget · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mesothelin (MSLN) may be the most "dramatic" of the tumor markers, being strongly overexpressed in nearly one-third of human malignancies. The biochemical cause is unclear. We previously ascribed this cancer-specific overexpression to an element, Canscript, residing around 50 bp 5' of the transcription start site in cancer (Hucl, T., Brody, J. R., Gallmeier, E., Iacobuzio-Donahue, C. A., Farrance, I. K., and Kern, S. E. (2007) Cancer Res. 67, 9055-9065). Herein, we found a Canscript promoter activity elevated over 100-fold in cancer cells. In addition to a highly conserved TEAD1 (TEA domain family member 1)-binding MCAT motif, nucleotide substitution revealed the consensus core sequence (WCYCCACCC) of an SP1-like motif in Canscript. The unknown transcription factor binding to the SP1-like motif may hold the key for the cancer specificity of Canscript. SP1, GLI1, and RUNX1, -2, and -3 appeared unlikely to be the direct transcription factors acting at the SP1-like motif, but KLF6 had some features of such a candidate. YAP1, a TEAD1-binding protein, appeared necessary, but not sufficient, for Canscript activity; knockdown of YAP1 by small interfering RNAs greatly reduced MSLN levels in MSLN-overexpressing cells, but overexpressing YAP1 in MSLN-negative cells did not induce MSLN expression. Cansript-like sequences were found in other genes up-regulated in pancreatic cancer; reporters driven by the sequences from FXYD3, MUC1, and TIMP1 had activities more than 2 times that of the control. This suggested that the cause of MSLN overexpression might also contribute mechanistically to the overexpression of other tumor markers.
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