REBACIN® inhibits E6/E7 oncogenes in clearance of human papillomavirus infection

Previous studies have demonstrated that REBACIN (R) intervention eliminates persistent high-risk human papillomavirus (hrHPV) infection. The initial establishment and subsequent progression of cervical cancer mainly depends on two major oncogenes, E6/E7, and previous studies have proposed E6/E7 oncogenes as a target for therapeutic drug development. The aim of this study was to investigate in vitro and in vivo whether REBACIN (R) inhibits E6/E7 oncogenes for elucidating the mechanism of REBACIN (R) in the clearance of persistent hrHPV infection. In vitro, after REBACIN (R) treatment, the growth of both Ca Ski and HeLa cervical cancer cells containing the E6/E7 oncogenes was prevented. In line with this finding is that E6/E7 expression was inhibited, which can be counteracted by the co-application of anti-REBACIN (R) antibody. These studies demonstrated that REBACIN (R) can effectively inhibit the growth of cervical cancer cells via targeting HPV E6/E7 expression. To further verify this finding in clinic, 108 volunteer patients with persistent hrHPV infections were randomly divided into REBACIN (R), recombinant human interferon alpha-2b (Immunological drug control), or no-treatment blank control groups, received intravaginal administration of REBACIN (R), interferon or no-treatment every other day for three months, and then followed up for E6/E7 mRNA assay. In REBACIN (R) group, 68.57% of patients showed complete clearance of HPV E6/E7 mRNA, which was significantly higher compared to 25.00% in the interferon immunological drug control group and 20.00% in blank control group, confirming that REBACIN (R) is potently efficacious on clearing persistent hrHPV infections via inhibition of HPV E6/E7 oncogenes.