Long non-coding RNA HOTAIR regulates proliferation, migration and invasion of human cervical cancer cells by modulating expression of MAPK1

Accumulating evidence suggests that long non-coding RNAs (lncRNAs) are dysregulated in cancer cells and may be responsible for the development and progression of this disease. Herein, the role and therapeutic potential of aberrantly expressed lncRNA HOTAIR were investigated in cervical cancer.

The expression profile of the lncRNA HOTAIR was determined by quantitative RT-PCR. CCK-8 and colony formation assays were used for determination of cell viability. DAPI and annexin V/PI assays were used for detection of apoptosis. Wound healing and transwell assays were used to monitor cell migration and invasion.

The results showed that the expression of lncRNA HOTAIR was significantly (p < 0.01) upregulated (up to 4.1-fold) in cervical cancer cell lines. Silencing of lncRNA HOTAIR expression resulted in inhibition of the proliferation of the DoTc2 cervical cancer cells via induction of apoptotic cell death. HOTAIR silencing also resulted in decrease of the migration and the invasive properties of the cervical cancer cells. HOTAIR has been reported to interact with MAPK1 in cancer cells, and in this study MAPK1 was found to be overexpressed (up to 3.7-fold) in all the cervical cancer cells and silencing of HOTAIR inhibited the expression of MAPK1 in DoTc2 cervical cancer cells. Silencing of MAPK1 in DoTc2 cells also inhibited their proliferation and metastasis via induction of apoptosis. Co-transfection experiments showed that silencing of MAPK1 and lncRNA HOTAIR causes inhibition of DoTc2 cell growth synergistically.

These results indicate that lncRNA HOTAIR may prove to be an important therapeutic target for management of cervical cancer.