Fig. 10: TIMM23 silencing results in impaired mitochondrial function, suppressed proliferation, and apoptotic cell death in pNSCLC-1 xenografts.
From: TIMM23 overexpression drives NSCLC cell growth and survival by enhancing mitochondrial function

Nude mice bearing pNSCLC-1 xenografts received intratumoral injections of either TIMM23 shRNA AAV (“shTIMM23-AAV”) or control shRNA AAV (“shC-AAV”) at 48-hour intervals for two consecutive rounds. Tumor volumes (A) and body weights of the animals (D) were monitored weekly. The estimated daily growth rate of pNSCLC-1 xenografts was calculated (B). At day 49 (“Day-49”), xenografts were excised and weighed individually (C). mRNA and protein expression levels were quantified in the indicated xenograft tissues (E, F, and L). Additionally, ATP content (G), the GSH/GSSH ratio (H), TBAR intensity (I) and cytosol cytochrome c content (K) in xenograft lysates were measured. Immunohistochemical staining was performed to evaluate nuclear Ki-67 incorporation (J) in the described xenograft tissue sections. TUNEL staining was conducted to detect apoptotic nuclei in the same tissue samples (M). Data were represented as mean ± standard deviation (SD). Statistical significance was determined by comparison to the aav-shC control group, with *P < 0.05 indicating significant differences and “N.S.” denoting non-significant differences (P > 0.05). Each experimental group comprised ten mice (n = 10) for panels A-D. For panels E-M, data were derived from five randomly selected tissue samples per xenograft (n = 5). Scale bars represent 100 µm.