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 inJournal of cellular physiology Vol. 234; no. 1; pp. 619 - 631
Main Authors Zhang, Hui, Zhang, Xuan, Li, Xun, Meng, Wen‐Bo, Bai, Zhong‐Tian, Rui, Shao‐Zhen, Wang, Zheng‐Feng, Zhou, Wen‐Ce, Jin, Xiao‐Da
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.01.2019
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ISSN0021-9541
1097-4652
1097-4652
DOI10.1002/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.
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
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  surname: Zhang
  fullname: Zhang, Hui
  organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province
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  surname: Zhang
  fullname: Zhang, Xuan
  organization: Northwest Minzu University
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  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
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  surname: Wang
  fullname: Wang, Zheng‐Feng
  organization: Key Laboratory of Biotherapy and Regenerative Medicine of Gansu Province
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  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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Keywords senescence
CCNB1
pancreatic cancer
p53 signaling pathway
cell cycle
gene silencing
apoptosis
Language English
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Notes Hui Zhang and Xuan Zhang are regarded as co‐first authors.
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PublicationTitle Journal of cellular physiology
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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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