Effect of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in pancreatic cancer
Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (C...
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Published in | Journal of cellular physiology Vol. 234; no. 1; pp. 619 - 631 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Wiley Subscription Services, Inc
01.01.2019
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ISSN | 0021-9541 1097-4652 1097-4652 |
DOI | 10.1002/jcp.26816 |
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Abstract | Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (CCNB1) expression has been detected in different cancers including PC. This study is designed to investigate the effects of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in PC. PC tissues and normal pancreatic tissues were collected. Cells were transfected and assigned into different groups. The expressions of CCNB1, p53, MDM2, Bax, caspase‐9, caspase‐3, and p21 in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. β‐Galactosidase staining, MTT assay, and flow cytometry were conducted to test cell senescence, proliferation, cell cycle, and apoptosis. PC tissues showed higher expressions of CCNB1 and MDM2 and lower expressions of Bax, caspase‐9, caspase‐3, and p21. Cells transfected with shCCNB1 had lower expressions of CCNB1 and MDM2, whereas higher expressions of Bax, caspase‐9, caspase‐3, p53, and p21. The shCCNB1 group had decreased proliferation and S‐phase cell proportion and increased apoptosis, senescence, and G0/G1‐phase cell proportion. The PFT‐α group showed higher expressions of MDM2 and lower expressions of Bax, caspase‐9, caspase‐3, p53, and p21. The PFT‐α group had increased proliferation and S‐phase cell proportion and declined apoptosis, senescence, and G0/G1‐phase cell proportion. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in PC.
CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in pancreatic cancer. |
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AbstractList | Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (CCNB1) expression has been detected in different cancers including PC. This study is designed to investigate the effects of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in PC. PC tissues and normal pancreatic tissues were collected. Cells were transfected and assigned into different groups. The expressions of CCNB1, p53, MDM2, Bax, caspase‐9, caspase‐3, and p21 in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. β‐Galactosidase staining, MTT assay, and flow cytometry were conducted to test cell senescence, proliferation, cell cycle, and apoptosis. PC tissues showed higher expressions of CCNB1 and MDM2 and lower expressions of Bax, caspase‐9, caspase‐3, and p21. Cells transfected with shCCNB1 had lower expressions of CCNB1 and MDM2, whereas higher expressions of Bax, caspase‐9, caspase‐3, p53, and p21. The shCCNB1 group had decreased proliferation and S‐phase cell proportion and increased apoptosis, senescence, and G0/G1‐phase cell proportion. The PFT‐α group showed higher expressions of MDM2 and lower expressions of Bax, caspase‐9, caspase‐3, p53, and p21. The PFT‐α group had increased proliferation and S‐phase cell proportion and declined apoptosis, senescence, and G0/G1‐phase cell proportion. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in PC. Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (CCNB1) expression has been detected in different cancers including PC. This study is designed to investigate the effects of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in PC. PC tissues and normal pancreatic tissues were collected. Cells were transfected and assigned into different groups. The expressions of CCNB1, p53, MDM2, Bax, caspase‐9, caspase‐3, and p21 in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. β‐Galactosidase staining, MTT assay, and flow cytometry were conducted to test cell senescence, proliferation, cell cycle, and apoptosis. PC tissues showed higher expressions of CCNB1 and MDM2 and lower expressions of Bax, caspase‐9, caspase‐3, and p21. Cells transfected with shCCNB1 had lower expressions of CCNB1 and MDM2, whereas higher expressions of Bax, caspase‐9, caspase‐3, p53, and p21. The shCCNB1 group had decreased proliferation and S‐phase cell proportion and increased apoptosis, senescence, and G0/G1‐phase cell proportion. The PFT‐α group showed higher expressions of MDM2 and lower expressions of Bax, caspase‐9, caspase‐3, p53, and p21. The PFT‐α group had increased proliferation and S‐phase cell proportion and declined apoptosis, senescence, and G0/G1‐phase cell proportion. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in PC. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in pancreatic cancer. Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (CCNB1) expression has been detected in different cancers including PC. This study is designed to investigate the effects of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in PC. PC tissues and normal pancreatic tissues were collected. Cells were transfected and assigned into different groups. The expressions of CCNB1, p53, MDM2, Bax, caspase-9, caspase-3, and p21 in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. β-Galactosidase staining, MTT assay, and flow cytometry were conducted to test cell senescence, proliferation, cell cycle, and apoptosis. PC tissues showed higher expressions of CCNB1 and MDM2 and lower expressions of Bax, caspase-9, caspase-3, and p21. Cells transfected with shCCNB1 had lower expressions of CCNB1 and MDM2, whereas higher expressions of Bax, caspase-9, caspase-3, p53, and p21. The shCCNB1 group had decreased proliferation and S-phase cell proportion and increased apoptosis, senescence, and G0/G1-phase cell proportion. The PFT-α group showed higher expressions of MDM2 and lower expressions of Bax, caspase-9, caspase-3, p53, and p21. The PFT-α group had increased proliferation and S-phase cell proportion and declined apoptosis, senescence, and G0/G1-phase cell proportion. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in PC.Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also, increasing evidence indicates that a panel of genes is newly identified in the pathogenesis of PC. As is a regulatory subunit, elevated cyclin B1 (CCNB1) expression has been detected in different cancers including PC. This study is designed to investigate the effects of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in PC. PC tissues and normal pancreatic tissues were collected. Cells were transfected and assigned into different groups. The expressions of CCNB1, p53, MDM2, Bax, caspase-9, caspase-3, and p21 in tissues and cells were detected by reverse transcription quantitative polymerase chain reaction and western blot analysis. β-Galactosidase staining, MTT assay, and flow cytometry were conducted to test cell senescence, proliferation, cell cycle, and apoptosis. PC tissues showed higher expressions of CCNB1 and MDM2 and lower expressions of Bax, caspase-9, caspase-3, and p21. Cells transfected with shCCNB1 had lower expressions of CCNB1 and MDM2, whereas higher expressions of Bax, caspase-9, caspase-3, p53, and p21. The shCCNB1 group had decreased proliferation and S-phase cell proportion and increased apoptosis, senescence, and G0/G1-phase cell proportion. The PFT-α group showed higher expressions of MDM2 and lower expressions of Bax, caspase-9, caspase-3, p53, and p21. The PFT-α group had increased proliferation and S-phase cell proportion and declined apoptosis, senescence, and G0/G1-phase cell proportion. CCNB1 silencing inhibits cell proliferation and promotes cell senescence via activation of the p53 signaling pathway in PC. |
Author | Zhang, Hui Li, Xun Bai, Zhong‐Tian Zhang, Xuan Meng, Wen‐Bo Rui, Shao‐Zhen Jin, Xiao‐Da Wang, Zheng‐Feng Zhou, Wen‐Ce |
Author_xml | – sequence: 1 givenname: Hui surname: Zhang fullname: Zhang, Hui organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 2 givenname: Xuan surname: Zhang fullname: Zhang, Xuan organization: Northwest Minzu University – sequence: 3 givenname: Xun surname: Li fullname: Li, Xun email: lxdr21@126.com organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 4 givenname: Wen‐Bo surname: Meng fullname: Meng, Wen‐Bo organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 5 givenname: Zhong‐Tian surname: Bai fullname: Bai, Zhong‐Tian organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 6 givenname: Shao‐Zhen surname: Rui fullname: Rui, Shao‐Zhen organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 7 givenname: Zheng‐Feng surname: Wang fullname: Wang, Zheng‐Feng organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 8 givenname: Wen‐Ce orcidid: 0000-0003-2573-9170 surname: Zhou fullname: Zhou, Wen‐Ce email: zhouwc129@163.com organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province – sequence: 9 givenname: Xiao‐Da surname: Jin fullname: Jin, Xiao‐Da organization: University of South China |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30069972$$D View this record in MEDLINE/PubMed |
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Snippet | Pancreatic cancer (PC) is a serious malignancy with high mortality and poor prognosis due to nonspecific incipient symptoms and early metastasis. Also,... |
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SubjectTerms | Apoptosis Cancer Caspase CCNB1 Cell activation Cell cycle Cell proliferation Cyclin B1 Cyclin-dependent kinase inhibitor p21 Flow cytometry Galactosidase gene silencing Malignancy MDM2 protein Metastases p53 Protein p53 signaling pathway Pancreatic cancer Pathogenesis Polymerase chain reaction Reverse transcription Senescence Signal transduction Signaling β-Galactosidase |
Title | Effect of CCNB1 silencing on cell cycle, senescence, and apoptosis through the p53 signaling pathway in pancreatic cancer |
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