ArticlePflugers Archiv : European journal of physiology2008
Upregulation of colonic ion channels in APC ( Min/+ ) mice.
Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Hyponatremia and Cancer Progression: Possible Association with Sodium-Transporting Proteins.Bioelectricity · 2020Article
- Cell volume regulation in cancer cell migration driven by osmotic water flow.Cancer science · 2019Review
- Expression Profiling of Calcium Channels and Calcium-Activated Potassium Channels in Colorectal Cancer.Cancers · 2019Article
- The Maxi-K (BK) Channel Antagonist Penitrem A as a Novel Breast Cancer-Targeted Therapeutic.Marine drugs · 2018Article
- MRP4 regulates ENaC-dependent CREB/COX-2/PGEOncotarget · 2017Article
- Long-term use of lithium and risk of colorectal adenocarcinoma: a nationwide case-control study.British journal of cancer · 2016Article
- Characterization of hERG1 channel role in mouse colorectal carcinogenesis.Cancer medicine · 2013Article
- Resting potential, oncogene-induced tumorigenesis, and metastasis: the bioelectric basis of cancer in vivo.Physical biology · 2012Article
- Enhanced suicidal erythrocyte death in mice carrying a loss-of-function mutation of the adenomatous polyposis coli gene.Journal of cellular and molecular medicine · 2012Article
- ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012Review
- Role of KCNMA1 in breast cancer.PloS one · 2012Article
- Tumor suppressor gene adenomatous polyposis coli downregulates intestinal transport.Pflugers Archiv : European journal of physiology · 2011Article
- Rapamycin inhibits oncogenic intestinal ion channels and neoplasia in APC(Min/+) mice.Oncogene · 2010Article
- Bioelectric controls of cell proliferation: ion channels, membrane voltage and the cell cycle.Cell cycle (Georgetown, Tex.) · 2009Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adenomatous polyposis coli (APC) tumor suppressor gene is mutated in almost all human colonic cancers. Disturbances in Na(+) absorption have been observed in colonic cancer, and ion channels such as ether a go-go (Eag) or Ca(2+)-sensitive BK channels have been recognized for their oncogenic potential. APC ( Min/+ ) mice have reduced APC expression and develop multiple intestinal neoplasias (Min). Ion channels in the colonic epithelium were examined using electrophysiology and molecular techniques. APC ( Min/+ ) mice developed intestinal neoplasia and experienced a significant weight loss. Due to intestinal bleedings, the hematocrit was largely reduced and plasma aldosterone levels were enhanced. Rectal potential measurements in vivo indicated an increase in amiloride-sensitive Na(+) absorption in APC ( Min/+ ) mice. Quantitative Ussing chamber studies demonstrated enhanced Na(+) absorption via epithelial Na(+) channels (ENaC) and suggested enhanced activity of oncogenic BK and Eag-1 channels. Patch clamp and fluorescence measurements on isolated crypts suggested enhanced K(+) channel activity in the surface epithelium. ENaC-mRNA and membrane protein expression was enhanced in colonic surface epithelial cells. The data suggest that reduced expression of the APC gene with upregulation of the downstream proteins Akt and mTOR and subsequent hyperaldosteronism is paralleled by upregulation of oncogenic potassium channels and enhanced colonic Na(+) absorption.
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