ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Molecular basis underlying inhibition of metastasis of gastric cancer by anti-VEGFa treatment.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- PAIP1 binds to pre-mRNA and regulates alternative splicing of cancer pathway genes including VEGFA.BMC genomics · 2024Article
- Syndecans and Pancreatic Ductal Adenocarcinoma.Biomolecules · 2021Review
- Mechanisms of Lower Extremity Vein Dysfunction in Chronic Venous Disease and Implications in Management of Varicose Veins.Vessel plus · 2021Article
- CircRhoC promotes tumorigenicity and progression in ovarian cancer by functioning as a miR-302e sponge to positively regulate VEGFA.Journal of cellular and molecular medicine · 2019Article
- Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease.Advances in pharmacology (San Diego, Calif.) · 2018Review
- Biochemical and Biological Attributes of Matrix Metalloproteinases.Progress in molecular biology and translational science · 2017Review
- Matrix Metalloproteinases in Remodeling of Lower Extremity Veins and Chronic Venous Disease.Progress in molecular biology and translational science · 2017Review
- Dapper homolog 1 alpha suppresses metastasis ability of gastric cancer through inhibiting planar cell polarity pathway.Oncotarget · 2016Article
- MiR-429 regulates gastric cancer cell invasiveness through ZEB proteins.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- miR-203 suppression in gastric carcinoma promotes Slug-mediated cancer metastasis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Fluorouracil induces autophagy-related gastric carcinoma cell death through Beclin-1 upregulation by miR-30 suppression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- MiR-153 regulates metastases of gastric cancer through Snail.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- YT521 promotes metastases of endometrial cancer by differential splicing of vascular endothelial growth factor A.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- miR-132 upregulation promotes gastric cancer cell growth through suppression of FoxO1 translation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- MiR-130b inhibits proliferation and induces apoptosis of gastric cancer cells via CYLD.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Isocitrate dehydrogenase 2 inhibits gastric cancer cell invasion via matrix metalloproteinase 7.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Matrix Metalloproteinases as Regulators of Vein Structure and Function: Implications in Chronic Venous Disease.The Journal of pharmacology and experimental therapeutics · 2015Review
- Impairment of growth of gastric carcinoma by miR-133-mediated Her-2 inhibition.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Promyelocytic leukemia protein enhances apoptosis of gastric cancer cells through Yes-associated protein.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Insulin-like growth factor 1 promotes growth of gastric cancer by inhibiting foxo1 nuclear retention.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
- Retraction · 2017-04-20Compromised Peer Review · Investigation by Journal/Publisher · · Journal published by SAGE starting in 2017
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neovascularization plays a substantial role in the invasiveness and metastasis of gastric cancer. However, the molecular mechanism underlying the control of neovascularization of gastric cancer remains undefined. Both vascular endothelial growth factor a (VEGFa) and matrix metalloproteinases 2 (MMP2) are essential for neovascularization by promoting endothelial mitogenesis and permeability and by promoting extracellular matrix degradation, respectively. Therefore, we were prompted to examine whether VEGFa and MMP2 may affect expression of each other to coordinate the neovascularization process. We found strong positive correlation of VEGFa and MMP2 levels in the gastric patients. Moreover, patients with metastasis of the original cancer had significantly higher levels of VEGFa and MMP2. Thus, we used a human gastric cancer cell line, SNU-5, to examine whether expression of VEGFa and MMP2 may affect each other. We found that overexpression of VEGFa in SNU-5 cells increased expression of MMP2, while inhibition of VEGFa in SNU-5 cells decreased expression of MMP2. On the other hand, overexpression of MMP2 in SNU-5 cells increased expression of VEGFa, while inhibition of MMP2 in SNU-5 cells decreased expression of VEGFa. These data suggest that expression of VEGFa and MMP2 may activate each other to reinforce a promoting effect on neovascularization. We then analyzed how VEGFa expression affects MMP2 level. Application of a specific Akt inhibitor to VEGFa-overexpressing SNU-5 cells substantially abolished the effect of VEGFa on MMP2 activation, suggesting that VEGFa may increase expression of MMP2 via PI3K/Akt signaling pathway. Since anti-VEGFa is a well-established therapy for many cancers, our data suggest that anti-VEGFa may not only inhibit neovascularization by prohibiting VEGFa-dependent endothelial mitogenesis and permeability increase but also by downregulating MMP2 to abolish the extracellular matrix degradation in gastric cancer.
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.