ABSTRACT
@#Objective: To investigate whether long non-coding RNA (lncRNA) FOXD2-AS1 targets miR-506-5p to regulate proliferation and apoptosis of cervical cancer cells. Methods: Human normal cervical cells Ect1/E6E7 and cervical cancer cell lines (HeLa, Siha and Caski) were cultured in vitro, and the expression levels of FOXD2-AS1 and miR-506-5p in cells were detected by qPCR. The cervical cancer cells with FOXD2-AS1 knockdown and miR-506-5p over-expression were constructed by liposome transfection technology, and the proliferation and apoptosis of cells were detected by MTT assay and flow cytometry respectively, the expression of proliferation-related proteins CyclinD1, p21, p27 and apoptosis-related proteins Bcl-2, BAX, cleaved-capase-3 were detected by WB. Dual luciferase reporter assay was used to verify whether FOXD2-AS1 would target miR-506-5p; and the effects of simultaneous inhibition of FOXD2-AS1 and miR-506-5p on proliferation and apoptosis of cervical cancer cells were also analyzed. Results: Compared with Ect1/E6E7 cells, the expression of FOXD2-AS1 significantly increased while the expression of miR-506-5p significantly decreased in cervical cancer HeLa, Siha and Caski cells (all P<0.01). FOXD2-AS1 knockdown significantly inhibited the protein expressions of CyclinD1, Bcl-2 and cell proliferationin cervical cancer cells, but promoted the protein expressions of p21, p27, BAX, cleavedcapase-3, and cell apoptosis (all P<0.01). miR-506-5p over-expression significantly inhibited the protein expressions of CyclinD1, Bcl2 and cell proliferation in cervical cancer cells, but promoted the protein expressions of p21, BAX, and cell apoptosis (all P<0.01). Dual luciferase reporter gene assay confirmed that FOXD2-AS1 negatively regulated the expression of miR-506-5p in cervical cancer cells (P<0.01). Inhibition of miR-506-5p expression reversed the effect of FOXD2-AS1 knockdown on proliferation and apoptosis of cervical cancer cell (P<0.01). Conclusion: FOXD2-AS1 modulates proliferation and apoptosis of cervical cancer cells by negatively regulating the expression of miR-506-5p.