Study on proliferation and apoptosis of cervical cancer HeLa cells by microRNA-506-3p targeting SPOCK1

  Objective  To explore the effect of miR-506-3p on proliferation and apoptosis of cervical cancer cell HeLa and its potential mechanism.

  Methods  Expressions of miR-506-3p and SPOCK1 mRNA in normal cervical cell Ect1/E6E7 as well as cervical cancer cells HeLa, Siha and Caski were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Double luciferase reporter assay was used to verify the possible target genes of miR-506-3p. The HeLa cell lines with miR-506-3p overexpression or SPOCK1 inhibition were established. MTT method was used to detecteHeLa cell proliferation activity, flow cytometry wasused to detect HeLa cell apoptosis rate, and western blot was used to detect the expression levels of SPOCK1, Cyclin D1, cyclinin kinase inhibitor (p21), B cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved-caspase3 and cleaved-PARP proteins.

  Results  Compared with Ect1/E6E7 cells, the expressions of miR-506-3p in cervical cancer cells HeLa, Siha and Caski were significantly lower, and the expressions of SPOCK1 mRNA were significantly higher (P < 0.05). SPOCK1 was the target gene of miR-506-3p. Overexpression of miR-506-3p or inhibition of SPOCK1 expression could inhibit HeLa cell proliferation, promote cell apoptosis, down-regulate the expression of Cyclin D1 and Bcl-2 proteins, up-regulate the expression of p21, Bax, cleaved-caspase3 and cleaved-PARP proteins (P < 0.05). Overexpression of SPOCK1 could partially reverse the effect of miR-506-3p overexpression on HeLa cells proliferation and apoptosis.

  Conclusion  The miR-506-3p can inhibit proliferation and promote apoptosis of cervical cancer cell HeLa by down-regulating SPOCK1 expression.