ArticleCell proliferation2004
Extracellular pressure stimulates colon cancer cell proliferation via a mechanism requiring PKC and tyrosine kinase signals.
Article in Cell proliferation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 41 citations in OpenAlex.
- Role of extrinsic physical cues in cancer progression.BMB reports · 2023Review
- Bioelectric Dysregulation in Cancer Initiation, Promotion, and Progression.Frontiers in oncology · 2022Review
- Regulation of Src Family Kinases during Colorectal Cancer Development and Its Clinical Implications.Cancers · 2020Review
- The Bioelectric Code: Reprogramming Cancer and Aging From the Interface of Mechanical and Chemical Microenvironments.Frontiers in cell and developmental biology · 2018Review
- Phosphorylation of Rab37 by protein kinase C alpha inhibits the exocytosis function and metastasis suppression activity of Rab37.Oncotarget · 2017Article
- Article
- Increased extracellular pressure stimulates tumor proliferation by a mechanosensitive calcium channel and PKC-β.Molecular oncology · 2015Article
- Article
- Long-term hydrocephalus alters the cytoarchitecture of the adult subventricular zone.Experimental neurology · 2014Article
- Quantitative stain-free and continuous multimodal monitoring of wound healing in vitro with digital holographic microscopy.PloS one · 2014Article
- Involvement of PKCα activation in TF/VIIa/PAR2-induced proliferation, migration, and survival of colon cancer cell SW620.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- Intestinal mucosal atrophy and adaptation.World journal of gastroenterology · 2012Review
- Influence of defunctionalization and mechanical forces on intestinal epithelial wound healing.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Effects of extracellular pressure and alcohol on the microglial response to inflammatory stimulation.American journal of surgery · 2012Article
- Changes in morphology and function in small intestinal mucosa after Roux-en-Y surgery in a rat model.The Journal of surgical research · 2012Article
- Isoform-specific modulation of pressure-stimulated cancer cell proliferation and adhesion by α-actinin.American journal of surgery · 2011Article
- Article
- The effects of mechanical forces on intestinal physiology and pathology.Cellular signalling · 2009Review
- Biological impact of mechanical stimuli on tumor metastasis.Cell cycle (Georgetown, Tex.) · 2009Article
- Increased extracellular pressure enhances cancer cell integrin-binding affinity through phosphorylation of beta1-integrin at threonine 788/789.American journal of physiology. Cell physiology · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledPressure in colonic tumours may increase during constipation, obstruction or peri-operatively. Pressure enhances colonocyte adhesion by a c-Src- and actin-cytoskeleton-dependent PKC-independent pathway. We hypothesized that pressure activates mitogenic signals.
methodsMalignant colonocytes on a collagen I matrix were subjected to 15 mmHg pressure. ERK, p38, c-Src and Akt phosphorylation and PKCalpha redistribution were assessed by western blot after 30 min and PKC activation by ELISA. Cells were counted after 24 h and after inhibition of each signal, tyrosine phosphorylation or actin depolymerization.
resultsPressure time-dependently increased SW620 and HCT-116 cell counts on collagen or fibronectin (P < 0.01). Pressure increased the SW620 S-phase fraction from 28 +/- 1 to 47 +/- 1% (P = 0.0002). Pressure activated p38, ERK, and c-Src (P < 0.05 each) but not Akt/PKB. Pressure decreased cytosolic PKC activity, and translocated PKCalpha to a membrane fraction. Blockade of p38, ERK, c-Src or PI-3-K or actin depolymerization did not inhibit pressure-stimulated proliferation. However, global tyrosine kinase blockade (genistein) and PKC blockade (calphostin C) negated pressure-induced proliferation.
conclusionsExtracellular pressure stimulates cell proliferation and activates several signals. However, the mitogenic effect of pressure requires only tyrosine kinase and PKCalpha activation. Pressure may modulate colon cancer growth and implantation by two distinct pathways, one stimulating proliferation and the other promoting adhesion.
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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 OpenQuestion graph.