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CBX3 promotes proliferation and regulates glycolysis via suppressing FBP1 in pancreatic cancer.
Chen, Lian-Yu; Cheng, Chien-Shan; Qu, Chao; Wang, Peng; Chen, Hao; Meng, Zhi-Qiang; Chen, Zhen.
Affiliation
  • Chen LY; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: lianyu_chen@hotmail.com.
  • Cheng CS; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: natcheng@qq.com.
  • Qu C; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: quchaolove@163.com.
  • Wang P; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: wangp413@163.com.
  • Chen H; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: chengkll@hotmail.com.
  • Meng ZQ; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: mengzhq@yeah.net.
  • Chen Z; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China; Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. Electronic address: zchenzl@fudan.edu.cn.
Biochem Biophys Res Commun ; 500(3): 691-697, 2018 06 07.
Article in En | MEDLINE | ID: mdl-29678579
ABSTRACT
More and more evidence has demonstrated that Chromobox protein homolog 3(CBX3) has an important role in carcinogenesis by regulating several mechanisms, such as heterochromatin formation, gene silencing, DNA replication and repair. However, its role in pancreatic cancer has seldom been discussed. In the present study, we silenced CBX3 expression in pancreatic cancer cell lines and identified the positive roles of CBX3 in cancer cell proliferation. Furthermore, we demonstrated that silencing CBX3 in pancreatic cancer cells inhibited aerobic glycolysis, the basis for providing cancer cells with building blocks for macromolecule synthesis and ATP that required. To search for the underlying molecular mechanism, we turned to examine the impact of CBX3 on the expression of FBP1, a negative regulator of aerobic glycolysis in pancreatic cancer and indicated that CBX3 negatively regulated FBP1 expression. Silencing FBP1 expression attenuated the decrease in glycolytic capacity that caused by CBX3 knockdown in pancreatic cancer cells. Taken together, these data reveal that CBX3 serves as a positive regulator of aerobic glycolysis via suppressing of the FBP1 in pancreatic cancer cells. Disrupting the CBX3-FBP1 signaling axis would be effective to treat pancreatic cancer and prevent aerobic glycolysis.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Pancreatic Neoplasms / Chromosomal Proteins, Non-Histone / DNA Helicases / DNA-Binding Proteins / Glycolysis Limits: Humans Language: En Journal: Biochem Biophys Res Commun Year: 2018 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Pancreatic Neoplasms / Chromosomal Proteins, Non-Histone / DNA Helicases / DNA-Binding Proteins / Glycolysis Limits: Humans Language: En Journal: Biochem Biophys Res Commun Year: 2018 Document type: Article
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