ArticleOncogene2007
Constitutively active CCK2 receptor splice variant increases Src-dependent HIF-1 alpha expression and tumor growth.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 39 citations in OpenAlex.
- Advances in the diagnosis and treatment of MET-variant digestive tract tumors.World journal of gastrointestinal oncology · 2024Review
- Targeted splicing therapy: new strategies for colorectal cancer.Frontiers in oncology · 2023Review
- Gastrin, Cholecystokinin, Signaling, and Biological Activities in Cellular Processes.Frontiers in endocrinology · 2020Review
- FUBP1 promotes neuroblastoma proliferation via enhancing glycolysis-a new possible marker of malignancy for neuroblastoma.Journal of experimental & clinical cancer research : CR · 2019Article
- hTERT mediates norepinephrine-induced Slug expression and ovarian cancer aggressiveness.Oncogene · 2015Article
- Distribution of cholecystokinin-B receptor genotype between patients with pancreatic cancer and controls and its impact on survival.Pancreas · 2015Article
- Somatic mutations in CCK2R alter receptor activity that promote oncogenic phenotypes.Molecular cancer research : MCR · 2012Article
- A single nucleotide polymorphism of the cholecystokinin-B receptor predicts risk for pancreatic cancer.Cancer biology & therapy · 2012Article
- Functional implications of structural predictions for alternative splice proteins expressed in Her2/neu-induced breast cancers.Journal of proteome research · 2011Article
- Expression of multiple forms of 3'-end variant CCK2 receptor mRNAs in human pancreatic adenocarcinomas.BMC research notes · 2011Article
- Article
- An antimicrobial peptide regulates tumor-associated macrophage trafficking via the chemokine receptor CCR2, a model for tumorigenesis.PloS one · 2010Article
- CCK(2) receptor splice variant with intron 4 retention in human gastrointestinal and lung tumours.Journal of cellular and molecular medicine · 2010Article
- CCK2 receptor expression transforms non-tumorigenic human NCM356 colonic epithelial cells into tumor forming cells.International journal of cancer · 2010Article
- Down-regulation of 20-HETE synthesis and signaling inhibits renal adenocarcinoma cell proliferation and tumor growth.Anticancer research · 2009Article
- Alternative splicing of pre-mRNA in cancer: focus on G protein-coupled peptide hormone receptors.The American journal of pathology · 2009Review
- Radiation-induced HIF-1alpha cell survival pathway is inhibited by soy isoflavones in prostate cancer cells.International journal of cancer · 2009Article
- Targeting of a CCK(2) receptor splice variant with (111)In-labelled cholecystokinin-8 (CCK8) and (111)In-labelled minigastrin.European journal of nuclear medicine and molecular imaging · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Gastrointestinal (GI) cancers ectopically express multiple splice variants of the cholecystokinin-2 (CCK(2))/gastrin receptor; however, their relative contributions to the cancer phenotype are unknown. The aim of this study was to compare the effects of CCK(2) receptor (CCK(2)R) and CCK(2i4sv)R expression on cell growth both in vitro and in vivo using a human epithelial cell model, HEK239. In vitro, receptor variant expression did not affect cell proliferation either in the absence or presence of agonist. However, in vivo, the expression of CCK(2i4sv)R, but not CCK(2)R, increases HEK293 tumor growth in a constitutive, Src-dependent manner. Enhanced tumorigenicity of CCK(2i4sv)R is associated with an Src-dependent increase in the transcription factor, hypoxia-inducible factor-1alpha, its downstream target, vascular endothelial growth factor and tumor micro-vessel density, suggesting that CCK(2i4sv)R may contribute to the growth and spread of GI cancers through agonist-independent mechanisms that enhance tumor angiogenesis.
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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.