ArticleJournal of cancer research and clinical oncology2013
siRNA-participated chemotherapy: an efficient and specific therapeutic against gastric cancer.
Article in Journal of cancer research and clinical oncology, 2013. 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 It has been retracted, and should not be counted.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 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Fibroblast growth factor receptor signaling as therapeutic targets in gastric cancer.World journal of gastroenterology · 2016Review
- Therapeutic targeting of fibroblast growth factor receptors in gastric cancer.Gastroenterology research and practice · 2015Review
- Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.American journal of cancer research · 2014Review
Corrections and comments
- Retraction · 2015-08-17Compromised Peer Review · Investigation by Journal/Publisher · Investigation by Third Party ·
- Retracted
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThis study aims to investigate the role of siRNA silencing fibroblast growth factor receptor (FGFR) expression in promoting chemotherapy effect of gastric cancer and to explore its mechanism.
methodsHuman gastric cancer cells MGC80-3 were divided into four groups: control group, cisplatin group (2 μg/L), cisplatin (2 μg/L) + siRNA group and siRNA group. The expressions of FGFR in four groups were detected by immunofluorescence. The cell proliferation and apoptosis were detected by MTT assay and flow cytometry. The protein expression levels of vascular endothelial growth factor receptor (VEGFR), caspase-3 and Bax were detected by Western blot. Further, animal model of gastric cancer was established and divided into four groups as in vitro experiment. The expression of FGFR mRNA in tumor tissue was detected by the real-time fluorescence quantitative polymerase chain reaction. The size of tumor was measured to analyze the effects of treatment. Histopathological detections were performed by hematoxylin and eosin staining and immunohistochemistry.
resultsFor in vitro experiment, significant decrease inFGFR expression, inhibition of proliferation and promotion of apoptosis were observed in siRNA-treated cells, so as cisplatin group. siRNA also resulted in the reduction of VEGFR and rise in apoptosis-related protein (caspase-3). As for the experiment in vivo, siRNA also suppressed the expression of FGFR and enhanced tumor shrink. Furthermore, the co-administration of siRNA and cisplatin revealed a more excellent antitumor effect than other therapies.
conclusionssiRNA can effectively suppress FGFR expression and cell proliferation, but promote apoptosis in vitro and also inhibit tumor growth and FGFR production in vivo. siRNA-participated chemotherapy may provide an efficient therapeutic approach to treat gastric cancer.
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.