ArticleOncogene2003
The PI 3-kinase-Rac-p38 MAP kinase pathway is involved in the formation of signet-ring cell carcinoma.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- Gastrointestinal signet ring cell malignancy: current advancement and future prospects.Investigational new drugs · 2023Review
- Current advances in understanding the molecular profile of hereditary diffuse gastric cancer and its clinical implications.Journal of experimental & clinical cancer research : CR · 2023Review
- Requirement for epithelial p38α in KRAS-driven lung tumor progression.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Signet-ring Cells in the Skin: A Case of Late-onset Cutaneous Metastasis of Gastric Carcinoma and a Brief Review of Histological Approach.Dermatology reports · 2016Article
- Scattering of MCF7 cells by heregulin ß-1 depends on the MEK and p38 MAP kinase pathway.PloS one · 2013Article
- Association between the TGFB1 -509C/T and TGFBR2 -875A/G polymorphisms and gastric cancer: a case-control study.Oncology letters · 2011Article
- Heregulin β-1 induces loss of cell-cell contact and enhances expression of MUC1 at the cell surface in HCC2998 and MKN45-1 cells.PloS one · 2011Article
- Carbonic anhydrase-related protein VIII increases invasiveness of non-small cell lung adenocarcinoma.Virchows Archiv : an international journal of pathology · 2006Article
- Induction of human NF-IL6beta by epidermal growth factor is mediated through the p38 signaling pathway and cAMP response element-binding protein activation in A431 cells.Molecular biology of the cell · 2005Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signet-ring cell carcinoma is classified in poorly differentiated adenocarcinoma with an aggressive nature and a poor prognosis. We have shown that the activation of PI 3-kinase in highly differentiated adenocarcinomas induces loss of cell-cell contact and formation of vacuoles, giving phenotypes similar to those of signet-ring cell lines. SB203580, a potent p38 MAP kinase inhibitor, blocked this transition, and expression of an active form of MKK6 (MKK6DA), an activator of p38 MAP kinase, gave effects similar to those induced by expression of the active form of PI 3-kinase (BD110), although formation of large vacuoles was not induced. Activation of MKK3, another activator of p38 MAP kinase, was activated in native signet-ring carcinoma cell lines. Anchorage-independent growth of signet-ring cell lines was inhibited by LY294002 or SB203580. These results suggest that p38 MAP kinase is functioning downstream of PI 3-kinase in signaling of the malignant phenotype. Secretion of mucins was enhanced in BD110-expressing cells, but not in MKK6DA-expressing cells, suggesting that secretion of mucins is independent of the MKK6-p38 MAP kinase cascade. Thus, there may be at least two pathways, p38 MAP kinase-dependent and -independent, which are involved in regulation of cell-cell contact and the protein secretion system, respectively.
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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 OpenQuestion graph.