ArticleBMC cancer2006
SSeCKS/Gravin/AKAP12 attenuates expression of proliferative and angiogenic genes during suppression of v-Src-induced oncogenesis.
Article in BMC cancer, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Interpreting the molecular mechanisms of RBBP4/7 and their roles in human diseases (Review).International journal of molecular medicine · 2024Review
- AKAP12 deficiency impairs VEGF-induced endothelial cell migration and sprouting.Acta physiologica (Oxford, England) · 2020Article
- SSeCKS/AKAP12 scaffolding functions suppress B16F10-induced peritoneal metastasis by attenuating CXCL9/10 secretion by resident fibroblasts.Oncotarget · 2017Article
- Functional cis-regulatory modules encoded by mouse-specific endogenous retrovirus.Nature communications · 2017Article
- The molecular effect of metastasis suppressors on Src signaling and tumorigenesis: new therapeutic targets.Oncotarget · 2015Review
- HIF-dependent regulation of AKAP12 (gravin) in the control of human vascular endothelial function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Digitoxin and its analogs as novel cancer therapeutics.Experimental hematology & oncology · 2012Article
- Temporal profile of Src, SSeCKS, and angiogenic factors after focal cerebral ischemia: correlations with angiogenesis and cerebral edema.Neurochemistry international · 2011Article
- Role for transcription factor TFII-I in the suppression of SSeCKS/Gravin/Akap12 transcription by Src.International journal of cancer · 2011Article
- Retinoid-induced expression and activity of an immediate early tumor suppressor gene in vascular smooth muscle cells.PloS one · 2011Article
- Re-expression of AKAP12 inhibits progression and metastasis potential of colorectal carcinoma in vivo and in vitro.PloS one · 2011Article
- Thioredoxin 1 enhances neovascularization and reduces ventricular remodeling during chronic myocardial infarction: a study using thioredoxin 1 transgenic mice.Journal of molecular and cellular cardiology · 2011Article
- Cellular processes of v-Src transformation revealed by gene profiling of primary cells--implications for human cancer.BMC cancer · 2010Article
- AKAP12 regulates human blood-retinal barrier formation by downregulation of hypoxia-inducible factor-1alpha.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Physiologic and pathophysiologic roles of AKAP12.Science progressArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSSeCKS is a major protein kinase C substrate with kinase scaffolding and metastasis-suppressor activity whose expression is severely downregulated in Src- and Ras-transformed fibroblast and epithelial cells and in human prostate, breast, and gastric cancers. We previously used NIH3T3 cells with tetracycline-regulated SSeCKS expression plus a temperature-sensitive v-Src allele to show that SSeCKS re-expression inhibited parameters of v-Src-induced oncogenic growth without attenuating in vivo Src kinase activity.
methodsWe use cDNA microarrays and semi-quantitative RT-PCR analysis to identify changes in gene expression correlating with i) SSeCKS expression in the absence of v-Src activity, ii) activation of v-Src activity alone, and iii) SSeCKS re-expression in the presence of active v-Src.
resultsSSeCKS re-expression resulted in the attenuation of critical Src-induced proliferative and pro-angiogenic gene expression including Afp, Hif-1alpha, Cdc20a and Pdgfr-beta, and conversely, SSeCKS induced several cell cycle regulatory genes such as Ptpn11, Gadd45a, Ptplad1, Cdkn2d (p19), and Rbbp7.
conclusionOur data provide further evidence that SSeCKS can suppress Src-induced oncogenesis by modulating gene expression downstream of Src kinase activity.
Indexed as
Identifiers
What OpenQuestion holds
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.