Downregulation of Krüppel‑like factor 1 inhibits the metastasis and invasion of cervical cancer cells

Mol Med Rep. 2018 Oct;18(4):3932-3940. doi: 10.3892/mmr.2018.9401. Epub 2018 Aug 20.

Abstract

Cervical cancer is one of the most common malignancies that seriously threatens women's health. Krüppel‑like factors (KLFs) have been reported to be associated with the progression of cervical cancer. The role of KLF1 in cervical cancer, which still remains unclear, was investigated in the present study. The expression of KLF1 was detected in different cervical cell lines by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting. Cell proliferation, metastasis and invasion were respectively detected by Cell Counting Kit‑8, wound healing and transwell assays. Associated factor expression was also detected by RT‑qPCR and western blotting. In addition, the phosphorylation levels of phosphatidylinositol‑3‑kinase (PI3K) and protein kinase B (Akt) were determined by western blot analysis. The results revealed that KLF1 expression was promoted in SiHa, Caski and C4‑1 cervical cancer cells. However, KLF1 knockdown suppressed cell proliferation, metastasis and invasion in SiHa cervical cancer cells. KLF1 knockdown also inhibited the expressions of Ki67, metastasis‑associated antigen 1 and matrix metalloproteinase (MMP)‑2. KLF1 knockdown promoted the expressions of nonmetastatic clone 23 type 1 and tissue inhibitor of metalloproteinase‑2, and the expression of MMP‑9 was promoted slightly as well. In addition, KLF1 knockdown inhibited the PI3K/Akt signaling pathway. Hence, it was concluded that KLF1 promoted metastasis and invasion via the PI3K/Akt signaling pathway in cervical cancer cells.

MeSH terms

  • Cell Line, Tumor
  • Cell Proliferation
  • Down-Regulation / genetics*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Kruppel-Like Transcription Factors / genetics*
  • Kruppel-Like Transcription Factors / metabolism
  • Neoplasm Invasiveness
  • Neoplasm Metastasis
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA Interference
  • Signal Transduction
  • Transfection
  • Uterine Cervical Neoplasms / genetics*
  • Uterine Cervical Neoplasms / pathology*

Substances

  • Kruppel-Like Transcription Factors
  • erythroid Kruppel-like factor
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt