Downregulation of Kr�ppel‑like factor 1 inhibits the metastasis and invasion of cervical cancer cells

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.

Krüppel-like factor 1 (KLF1) promoted the proliferation, migration and invasion of human lens epithelial cells by enhancing the expression of Zinc Finger and BTB Domain Containing 7A (ZBTB7A) and activating Wnt/β-catenin pathway

“…It has been reported that the expression of KLF1 enhanced the proliferation, migration and invasion of cervical cancer cells [ 9 ]. Moreover, some study revealed that KLF1 promoted the proliferation and invasiveness of breast cancer cells by activating the EMT process [ 26 ].…”

“…Moreover, KLF1 is highly expressed in a variety of tumors, such as cervical cancer. The expression of KLF1 promoted the proliferation and EMT of cervical cancer cells by activating PI3K/Akt pathway [ 9 ]. KLF1 is also associated with drug resistance of ovarian cancer cells [ 10 ].…”

Krüppel-like factors in tumors: Key regulators and therapeutic avenues

“…Several other KLFs also participate in the regulation of PI3K/AKT signaling. KLF1 promotes metastasis and invasion via the PI3K/AKT signaling pathway in cervical cancer cells by enhancing the phosphorylation levels of PI3K and AKT ( 41 ). KLF10 inhibits melanoma cells’ proliferation, invasion, and migration by upregulating acyl−CoA medium−chain synthetase 3.…”

KLF16 Downregulates the Expression of Tumor Suppressor Gene TGFBR3 to Promote Bladder Cancer Proliferation and Migration

“…Downregulation of KLF1 can inhibit the invasion and migration ability of cervical cancer cells. 10 KLF3 shows a high expression trend in lung cancer patients, and reducing KLF3 expression can inhibit the growth and migration of lung cancer cells. 11 KLF16 also plays a role in tumor growth and metastasis.…”