ArticleOncology letters2017
Treatment with the herbal formula Songyou Yin inhibits epithelial-mesenchymal transition in hepatocellular carcinoma through downregulation of TGF-β1 expression and inhibition of the SMAD2/3 signaling pathway.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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
5 citing papers in PubMed, 11 citations in OpenAlex.
- Article
- The Role of TGF-β/SMAD Signaling in Hepatocellular Carcinoma: from Mechanism to Therapy and Prognosis.International journal of biological sciences · 2024Review
- Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis.Molecular medicine reports · 2021Article
- Su Yang Decoction induces human colon carcinoma cell apoptosis by activating caspases.Oncology letters · 2019Article
- Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin.International journal of molecular medicine · 2018Article
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It was previously reported that treatment with the herbal formula Songyou Yin (SYY) may serve a role in attenuating epithelial-mesenchymal transition (EMT). In the present study, the effect of treatment with SYY on transforming growth factor-β1 (TGF-β1)-induced EMT was investigated and the potential underlying molecular mechanisms were evaluated. MHCC97H cells were pretreated with SYY for 4 weeks and subsequently named MHCC97HSYY cells. Simultaneously, MHCC97H cells were cultured for 4 weeks without SYY and used as a negative control. Western blot analysis and enzyme-linked immunosorbent assays demonstrated that treatment with SYY inhibited EMT-associated changes and TGF-β1 expression in MHCC97H cells. MHCC97H and MHCC97HSYY cells were treated with 10 ng/ml TGF-β1 to induce EMT. The results of the present study demonstrated that pretreatment with SYY markedly inhibited TGF-β1-induced morphological changes, and reversed the expression of the EMT markers E-cadherin and N-cadherin. In addition, expression levels of the TGF-β1 downstream proteins, phosphorylated mothers against decapentaplegic homologs (p-SMAD)2 and 3, were reduced. Transwell assays indicated that pretreatment with SYY inhibited TGF-β1-induced cancer cell invasion and migration. The results of the present study indicate that SYY inhibited EMT through attenuation of TGF-β1 expression, and downregulation of p-SMAD2 and 3.
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Registered trials
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