ArticleWorld journal of gastroenterology2009
Treatment of chronic proliferative cholangitis with c-myc shRNA.
Article in World journal of gastroenterology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Management of Hepatolithiasis: Review of the Literature.Current gastroenterology reports · 2020Review
- EGFR monoclonal antibody panitumumab inhibits chronic proliferative cholangitis by downregulating EGFR.International journal of molecular medicine · 2019Article
- Lipopolysaccharide stimulates endogenous β-glucuronidase via PKC/NF-κB/c-myc signaling cascade: a possible factor in hepatolithiasis formation.Molecular and cellular biochemistry · 2018Article
- Effects of C-myc gene silencing on interleukin-1β-induced rat chondrocyte cell proliferation, apoptosis and cytokine expression.Journal of bone and mineral metabolism · 2018Article
- Selective gene silencing by viral delivery of short hairpin RNA.Virology journal · 2010Review
- Significance of controlling chronic proliferative cholangitis in the treatment of hepatolithiasis.World journal of surgery · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the feasibility and effectiveness of c-myc shRNA in inhibiting the hyperplastic behavior and lithogenic potentiality of chronic proliferative cholangitis (CPC), in order to prevent stone recurrence and biliary restenosis.
methodsAn animal model of CPC was established by giving intralumenally 0.5 mL of c-myc shRNA. Then, the effects of c-myc shRNA on hyperplastic behavior and lithogenic potentiality of CPC were evaluated by histological observation, immunohistochemistry, real-time PCR and Western blotting for c-myc, proliferating cell nuclear antigen (PCNA), procollagen III, mucin 5AC, enzymatic histochemistry for beta-glucuronidase, and biochemistry for hydroxyproline in the diseased bile duct.
resultsTreatment with c-myc shRNA efficiently suppressed the hyperplasia of biliary epithelium, submucosal gland, and collagen fiber by inhibiting mRNA and protein expression of c-myc. More importantly, it decreased the lithogenic potentiality of CPC by inhibiting the expression of mucin 5AC and the secretion of endogenous beta-glucuronidase. Further investigation indicated that c-myc shRNA-3 had a better inhibitory effect on CPC.
conclusionTreatment with c-myc shRNA-3 can control CPC and reduce the lithogenic potentiality of CPC.
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Registered trials
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