ArticleInternational journal of clinical and experimental pathology2015
Silencing of ZNF139-siRNA induces apoptosis in human gastric cancer cell line BGC823.
Article in International journal of clinical and experimental pathology, 2015. 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, 16 citations in OpenAlex.
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- Zinc Finger Proteins in the War on Gastric Cancer: Molecular Mechanism and Clinical Potential.Cells · 2023Review
- MCM3AP-AS1 regulates proliferation, apoptosis, migration, and invasion of breast cancer cells via binding with ZFP36.Translational cancer research · 2021Article
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- Role of the zinc finger and SCAN domain-containing transcription factors in cancer.American journal of cancer research · 2019Review
- Zinc Finger Protein 521, Negatively Regulated by MicroRNA-204-5p, Promotes Proliferation, Motility and Invasion of Gastric Cancer Cells.Technology in cancer research & treatment · 2019Article
- Condition-adaptive fused graphical lasso (CFGL): An adaptive procedure for inferring condition-specific gene co-expression network.PLoS computational biology · 2018Article
- MicroRNA-421 promotes the proliferation and metastasis of gastric cancer cells by targeting claudin-11.Experimental and therapeutic medicine · 2017Article
- ZKSCAN1 gene and its related circular RNA (circZKSCAN1) both inhibit hepatocellular carcinoma cell growth, migration, and invasion but through different signaling pathways.Molecular oncology · 2017Article
- Zinc finger proteins in cancer progression.Journal of biomedical science · 2016Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeZNF139, a member of zinc finger protein family, is a transcription factor. Our previous studies have showed that the over-expression of ZNF139 in gastric cancer (GC) cells was related to the differentiation of GC. However, the function of ZNF139 in GC cells' apoptosis is still unclear. In present study, endogenous ZNF139 in GC cell line BGC823 was inhibited with siRNA, and then mechanism of ZNF139 in GC cells' apoptosis was investigated.
methodsExpression of ZNF139 in GC tissues, adjacent normal tissues, GC cell lines MKN28, SGC7901, BGC823 and that in gastric epithelial cell line GES-1 were tested. Then ZNF139-specific siRNA was transfected into BGC823 cells. Viability, cell cycle and apoptosis of GC cells were detected. Survivin, x-IAP, caspase-3, Fas, p53, Bcl-2 and Bax genes were detected with QPCR and Western blot.
resultsZNF139 expression in GC tissues was significantly higher than that in adjacent normal tissues; ZNF139 expression in GES-1 was very weak, but it expressed in various GC cell lines, with the highest expression in BGC823. After endogenous ZNF139 was inhibited with ZNF139-siRNA, FCM indicated that after transfection, GC cells in G0/G1 phase was significantly increased, but was significantly reduced in G2/M phases; also after transfection, the apoptotic rate of BGC823 cells increased significantly. 48 h after ZNF139-siRNA was transfected, the expression of Survivin, x-IAP and Bcl-2 was significantly down-regulated, while the expression of caspase-3 and Bax was significantly up-regulated.
conclusionOur results suggest that ZNF139 functions to promote apoptosis resistance of BGC823 by regulating some apoptosis related genes.
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Identifiers
26722429PMC4680374W2419127979What OpenQuestion holds
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