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.