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Neoplasma Vol.67, No.6, p.1223–1232, 2020 |
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Title: Downregulation of CDCA3 expression inhibits tumor formation in pancreatic cancer | ||
Author: R. C. ZOU, Z. T. GUO, D. WEI, Z. T. SHI, Z. C. YE, G. ZHAI, C. ZHONG, B. TANG, L. WANG, J. Y. GE | ||
Abstract: Downregulation of cell division cycle-associated 3 (CDCA3) markedly inhibited cell growth and induced apoptosis in tumors. However, the effect of CDCA3 in pancreatic cancer (PAC) was rarely investigated. Therefore, this study attempted to clarify the role of CDCA3 in PAC. The mRNA and protein expression of CDCA3 were examined in PAC cell lines and tumor tissues by using real-time quantitative PCR (RT-qPCR), western blotting (WB), and immunohistochemistry (IHC). The effects of CDCA3 downregulation on cell proliferation, apoptosis, and colony information were investigated through MTT assay, Annexin V-APC single staining cell apoptosis detection, and colony formation test. The microarray and ingenuity pathway analysis were employed to explore the potential regulatory relation. The tumor xenograft model was established for determining the effect of CDCA3 downregulation on the growth of PAC in vivo. The results showed that the expression of CDCA3 in tumor tissues was higher than that of normal tissues (pwhen compared with human pancreatic duct epithelial (HPDE) cells (p and SW 1990 cells was significantly inhibited after the lentivirus transfection of CDCA3 knockdown (pin the shCDCA3 group compared to that in the shCtrl group in SW 1990 cells and PANC-1 cells (pared to the shCtrl group (p was notably inhibited in the shCDCA3 group relative to the shCtrl group in SW 1990 cells (ph the shCtrl group in vivo (pd that CDCA3 plays a crucial role in the progress of PCA by regulating cell apoptosis and proliferation, which may serve as a potential target for PAC treatment. |
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Keywords: cell division cycle-associated 3; pancreatic neoplasms; cell proliferation; apoptosis | ||
Published online: 23-Jul-2020 | ||
Year: 2020, Volume: 67, Issue: 6 | Page From: 1223, Page To: 1232 | |
doi:10.4149/neo_2020_200411N388 |
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