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Knockdown EIF3C Suppresses Cell Proliferation and Increases Apoptosis in Pancreatic Cancer Cell
- Source :
- Dose-Response, Vol 18 (2020), Dose-Response
- Publication Year :
- 2020
- Publisher :
- SAGE Publishing, 2020.
-
Abstract
- Increasing evidence shows that eukaryotic initiation factor subunit (EIF3C) plays a crucial role in development of tumors. However, the underlying roles of EIF3Cin the development of pancreatic cancer (PC) remain unknown. In this study, we examined the expression of EIF3C in PC tissues, their adjacent normal tissues and 3 cell lines (SW1990, PANC-1 and AsPC-1). Moreover, the EIF3C-shRNA lentivirus was constructed to suppress EIF3C expression. Following this, the cell colony formation assay was employed to evaluate proliferation ability of PC cells. Meanwhile, the cell cycle and apoptotic assays were also performed by flow cytometry. We found that level of EIF3C in PC tissues was significantly increased compared with that in adjacent normal tissues. Furthermore, the knockdown of EIF3C can significantly reduce cell proliferation, block cell cycle in G2/M and induce apoptosis in both SW1990 and PANC-1 cells. Our findings suggest that EIF3C plays a crucial role in the progression of PC and may be a potential target in the treatment of PC.
- Subjects :
- 0301 basic medicine
Health, Toxicology and Mutagenesis
Cell
Toxicology
Flow cytometry
03 medical and health sciences
PANC-1 cells
0302 clinical medicine
Eukaryotic initiation factor
medicine
pancreatic adenocarcinoma
Gene knockdown
Chemical Health and Safety
medicine.diagnostic_test
Cell growth
Chemistry
eukaryotic initiation factor subunit
SW1990 cells
lcsh:RM1-950
Public Health, Environmental and Occupational Health
Cell cycle
Cell biology
030104 developmental biology
medicine.anatomical_structure
lcsh:Therapeutics. Pharmacology
Cell culture
Apoptosis
030220 oncology & carcinogenesis
Original Article
Subjects
Details
- Language :
- English
- ISSN :
- 15593258
- Volume :
- 18
- Database :
- OpenAIRE
- Journal :
- Dose-Response
- Accession number :
- edsair.doi.dedup.....a0d24e6681b3b1d5f6e09a105e23bd5d