Long non-coding RNA NKILA regulates expression of HSP90 alpha, NF-kappa B and beta-catenin proteins in the MCF-7 breast cancer cell line

Abstract

Non-coding RNAs are increasingly being investigated and have shown great potential for diagnosis, prognosis and treatment of cancer. Thus, we have investigated a possible regulatory mechanism between NF-kappa B suppressor-NKILA, and HSP90, NF-kappa B, and beta-catenin molecules in MCF-7 breast cancer cells. HSP90 is an important stress protein and together with beta-catenin and NF-kappa B molecules can be responsible for cancer cell development. However, there is no comprehensive data available on the novel molecule NKILA unlike for HSP90, beta-catenin and NF-kappa B alone. Therefore, we suggest there might be a correlation between NKILA and these proteins. To investigate the NKILA role on HSP90, NF-kappa B and beta-catenin proteins we inhibited the NKILA by using transfection in MCF-7 breast cancer cells. NKILA-siRNA transfected cells were incubated for 5 h. Then, cells were collected and proteins were extracted to be separated by SDS-PAGE. The aforementioned proteins of siRNA transfected group were evaluated by quantification and comparison of their relative expression levels with the control group by immunoblotting. Results showed, HSP90 and NF-kappa B/p105, NF-kappa B/p65 and NF-kappa B/p50 subunits significantly increased while the level of beta-catenin decreased after NKILA inhibition. For the first time we have demonstrated that HSP90 and expression levels of beta-catenin are associated with NKILA levels which may be closely related to the canonical NF-kappa B pathway in MCF-7 cells. These novel findings may have significant implications in cancer cells development and possibly present important hints for the future studies of the cancer cell targeted therapy.