Upregulation of CENPM facilitates tumor metastasis via the mTOR/p70S6K signaling pathway in pancreatic cancer

Oncol Rep. 2020 Sep;44(3):1003-1012. doi: 10.3892/or.2020.7673. Epub 2020 Jul 7.

Abstract

Pancreatic cancer is a severe disease with high morbidity and mortality. However, the primary molecular mechanisms of pancreatic tumor formation and progression remain unclear. The present study using sequencing technology revealed that the centromere protein M (CENPM) gene was overexpressed in pancreatic cancer tissues. CENPM is one of the components of a complex that plays a central role in kinetochore protein assembly, mitotic progression and chromosome segregation. However, the biological function of CENPM in pancreatic cancer has yet to be determined. Hence, two effective siRNAs were designed to knock down CENPM. Notably, downregulation of CENPM inhibited pancreatic cancer cell proliferation, altered the cell cycle and limited pancreatic cancer cell migration and invasion via the mTOR/p70S6K signaling pathway. This research provides new evidence that CENPM overexpression plays a significant role in the progression of pancreatic cancer. Overall, the present findings indicated that CENPM may be a significant biomarker for predicting the development and progression of pancreatic malignancy.

Keywords: pancreatic cancer; CENPM; metastasis; mTOR/p70S6K signaling pathway.

MeSH terms

  • Biomarkers, Tumor / genetics*
  • Biomarkers, Tumor / metabolism
  • Carcinoma, Pancreatic Ductal / genetics*
  • Carcinoma, Pancreatic Ductal / mortality
  • Carcinoma, Pancreatic Ductal / secondary
  • Case-Control Studies
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Computational Biology
  • Datasets as Topic
  • Disease-Free Survival
  • Gene Expression Regulation, Neoplastic
  • Gene Knockdown Techniques
  • Humans
  • Pancreas / pathology
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / mortality
  • Pancreatic Neoplasms / pathology
  • RNA, Small Interfering / metabolism
  • RNA-Seq
  • Ribosomal Protein S6 Kinases, 70-kDa
  • Signal Transduction / genetics
  • Survival Rate
  • TOR Serine-Threonine Kinases / metabolism
  • Time Factors
  • Up-Regulation

Substances

  • Biomarkers, Tumor
  • CENPM protein, human
  • Cell Cycle Proteins
  • RNA, Small Interfering
  • MTOR protein, human
  • Ribosomal Protein S6 Kinases, 70-kDa
  • TOR Serine-Threonine Kinases