Research Paper Volume 12, Issue 10 pp 9604—9620

KMT2A regulates cervical cancer cell growth through targeting VDAC1

Figure 6. KMT2A knockdown inhibited cervical cancer growth in a mouse xenograft model. The control shRNA (shNC), KMT2A-shRNA (sh1), KMT2A-shRNA + VDAC1 overexpression (sh1+VDAC1), empty vector (Vector) and KMT2A overexpression plasmid (KMT2A) were intratumorally injected into mice. (A and B) Representative photographs of the tumor bearing mice and morphology of tumor xenograft from each mouse. (C and D) The average tumor volume and the average tumor weight of each group with KMT2A knockdown (C) and KMT2A overexpression (D). (E and F) The tumor volume of each mouse was measured and recorded every three days and body weight of each mouse was monitored every three days with KMT2A knockdown (E) and KMT2A overexpression (F). (G) The expression of the proteins in tumor xenografts were tested by immunohistochemical staining. (400× magnification).