REBACIN® inhibits expression of oncogenes E6/E7
In both TC-1 and HeLa cell lines stably expressing E6/E7 oncogenes, the mRNA transcription of HPV E6/E7 was markedly inhibited by the application of REBACIN®.13 In TC-1 cells, a low concentration of 19 μg/mL REBACIN®significantly inhibited E6 expression, whereas 78 μg/mL REBACIN® had a clear effect on the inhibition of E7 expression (also see the overview in Figure 1A and 1B). Similarly, in HeLa cells, 78 μg/mL REBACIN® markedly prevented E6 expression, whereas 19 μg/mL REBACIN® decreased E7 expression. In a clinical observation, one course (three months) of REBACIN® treatment remarkably reduced E6/E7 mRNA in hrHPV-infected patients, most of which became negative (see overview Figure 1C).14 Consistent with this clinical observation in a case report, another clinical observation study demonstrated that after one course of treatment, 68.57% of patients showed complete suppression of HPV E6/E7 mRNA expression in the REBACIN® group and 20% in the control group.19 In protein level, REBACIN®was also found to significantly inhibit the expression of HPV16 oncoprotein E7 in a dose-dependent (see overview Figure 1D)14 and time-dependent manner19. All in vitro, in vivo, and clinical studies have demonstrated and confirmed that REBACIN® effectively targets and inhibits the expression of viral E6/E7 oncogenes, thereby demonstrating that REBACIN® may play a key role in clearing persistent hrHPV infection and in the regression of associated cervical epithelial lesions.
REBACIN® impedes growth ofcervical cancer cells
REBACIN® specifically inhibited the growth of cervical cancer cells of Ca Ski via inhibiting viral oncoprotein E6/E7 expression, and anti-REBACIN® antibody counteracted this inhibitory effect, but had no significant effect on the growth of 293T cells lacking the E6 and E7 genes (Figure 2A and 2B).19 These findings demonstrated that REBACIN® can specifically target and inhibit the expression of hrHPV E6/E7 oncogenes.