NF‑κB interaction long non‑coding RNA inhibits migration, invasion and epithelial‑mesenchymal transition of cervical cancer cells through inhibiting NF‑κB signaling pathways
- Feipeng Wang
- Xiaochun Jiang
- Pei Wang
Affiliations: Department of Gynaecology, Xianyang Central Hospital, Xianyang, Shaanxi 712000, P.R. China
- Published online on: May 14, 2020 https://doi.org/10.3892/etm.2020.8752
Copyright: © Wang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
The long non-coding RNA (lncRNA) NF‑κB interaction lncRNA (NKILA) has been found to exert tumor suppressive effects in numerous types of carcinoma; however, the relationship between NKILA and cervical cancer (CC) remains largely unclear. The present study aimed to investigate the effects of NKILA on the proliferation and metastasis of CC cell lines, in addition to the related molecular mechanisms. Reverse transcription‑quantitative PCR was used to detect the expression levels of NKILA in cancer tissues and cell lines. The constructed overexpression vector, pcDNA3.1NKILA, and its corresponding negative control sequence were transfected into CaSki cells and short hairpin RNA targeting NKILA and the corresponding negative control sequence were transfected into C‑33A cells. Subsequently, the proliferative, migratory and invasive ability, as well as the process of epithelial‑mesenchymal transition (EMT) of C‑33 A and CaSki cells were analyzed by performing Cell Counting Kit‑8, wound healing, Matrigel invasion and western blot assays, respectively. The expression levels of proteins were detected using western blot analysis. The expression levels of NKILA were decreased in CC tissues and CC cell lines (SiHa, C‑33A, CaSki and HeLa) and the downregulation of NKILA expression using shRNA was observed to significantly increase the proliferation of CC cells. Conversely, the upregulation of NKILA inhibited the proliferation of CC cells, in addition to significantly inhibiting the migration and invasion of CaSki cells, whereas the knockdown of NKILA promoted the invasion of C‑33A cells. Thus, it was hypothesized that NKILA may inhibit the migration and invasion of CC cells via regulation of EMT processes, which was reflected by the expression of ZO‑1, E‑cadherin, N‑cadherin and Vimentin. Furthermore, the overexpression of NKILA significantly inhibited the activation of NF‑κB in CaSki cells, whereas the knockdown of NKILA expression promoted the degradation of inhibitory protein‑κB and promoted the transfer of p65 into the nucleus in C‑33A cells. In conclusion, the results from the present study suggested that NKILA may be involved in the inhibition of migration and invasion in CC cells through regulating EMT processes, which may be related to its inhibition of NF‑κB activation.