ArticleFEBS open bio2016
SNAI1 promotes the development of HCC through the enhancement of proliferation and inhibition of apoptosis.
Article in FEBS open bio, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- Article
- miR-34a-5p might have an important role for inducing apoptosis by down-regulation of SNAI1 in apigenin-treated lung cancer cells.Molecular biology reports · 2021Article
- Prognostic and Predictive Value of Transcription Factors Panel for Digestive System Carcinoma.Frontiers in oncology · 2021Article
- Circular RNAs: epigenetic regulators in cancerous and noncancerous skin diseases.Cancer gene therapy · 2020Review
- Controversies around epithelial-mesenchymal plasticity in cancer metastasis.Nature reviews. Cancer · 2019Review
- miR-30a regulates the proliferation and invasion of breast cancer cells by targeting Snail.Oncology letters · 2019Article
- Knockdown of BRCC3 exerts an anti‑tumor effect on cervical cancer in vitro.Molecular medicine reports · 2018Article
- The E3 ubiquitin ligase MuRF2 attenuates LPS-induced macrophage activation by inhibiting production of inflammatory cytokines and migration.FEBS open bio · 2018Article
- MAPK/p38 regulation of cytoskeleton rearrangement accelerates induction of macrophage activation by TLR4, but not TLR3.International journal of molecular medicine · 2017Article
- Synaptotagmin-7 is overexpressed in hepatocellular carcinoma and regulates hepatocellular carcinoma cell proliferation via Chk1-p53 signaling.OncoTargets and therapy · 2017Article
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Authors and funding
9 authors.
Funding
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Abstract
SNAI1, a zinc-finger transcription factor, plays an important role in the induction of epithelial-mesenchymal transition (EMT) in various cancers. However, the possible functions of SNAI1 in the proliferation and apoptosis of hepatocellular carcinoma have not been clearly identified. In this study, we investigated the effects and mechanisms of SNAI1 in the proliferation and apoptosis of hepatocellular carcinoma using clinical samples and cell lines. We found that SNAI1 is highly expressed in the tissues of liver cancer compared with adjacent nontumor tissues. SNAI1 is also highly expressed in the hepatoma cell lines HepG2, SMMC-7721, and BEL-7402 compared with the human normal liver cell line L02. We also observed that SNAI1 expression was correlated with distal metastasis, incomplete tumor capsule formation, and histological differentiation in hepatocellular carcinoma (HCC). Moreover, we demonstrated that knockdown of SNAI1 via lentiviral vectors of RNAi against SNAI inhibited cell proliferation by inducing G1 arrest, which was accompanied by the downregulation of cyclin D1 but not that of cyclin A. In addition, knockdown of SNAI1 promoted apoptosis by decreasing the expression of Bcl-2. In conclusion, our findings revealed that SNAI1 is involved in the development of hepatocellular carcinoma via regulating the growth and apoptosis of tumor cells.
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