p68 prompts the epithelial‑mesenchymal transition in cervical cancer cells by transcriptionally activating the TGF‑β1 signaling pathway
- Ming‑Yi Li
- Jin‑Quan Liu
- Dong‑Ping Chen
- Zhou‑Yu Li
- Bin Qi
- Wen‑Jing Yin
- Lu He
Published online on: December 8, 2017
Copyright: © Li et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
Overexpression of p68 has been reported in various types of cancer. However, little study has been conducted on the expression and role of p68 in cervical cancer. Therefore, the present study focuses on the role of p68 in cervical cancer cells, which may elucidate its potential mechanism of cervical cancer progression and shed light on the precision medical treatment of cervical cancer. Firstly, the expression of p68 was analyzed using reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The changes to cell morphology were observed using an inverted microscope (XDS‑500D; Shanghai Caikon Optical Instrument Co., Ltd., Shanghai, China). Cell migration was determined using an in vitro scratch assay. The present study demonstrated that the mRNA and protein levels of p68 were significantly enhanced in cervical cancer CaSki, HeLa [human papillomavirus (HPV)‑18‑positive], SiHa (HPV‑16‑positive) and C‑33A (HPV‑negative) cell lines compared with the human keratinocyte HaCaT cell line. Overexpression of p68 induced an elongated and spindle‑shaped morphology in CaSki cells. Upregulation of p68 increased the expression of α‑smooth muscle actin, vimentin and fibronectin however, epithelial marker E‑cadherin was significantly decreased. Furthermore, the in vitro scratch assay demonstrated that overexpression of p68 markedly enhanced CaSki cell migration capacity at 24 and 48 h. Knockdown of p68 partially reversed transforming growth factor‑β1 (TGF‑β1)‑induced changes in epithelial‑mesenchymal transition (EMT) markers and cell morphological changes. In summary, the present study demonstrated that p68 transcriptionally activated the expression of TGF‑β1, thereby prompting EMT in cervical cancer cells.