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Figure 7. KLF5 drives tumor growth and suppresses oxaliplatin efficacy in KRAS-mutant CRC in vivo. (A and B) Xenograft tumor model established by injecting KRAS-mutant CRC cells into nude mice. Tumor volumes were calculated and plotted at the indicated time points (mean ± SEM); (C and D) KLF5 overexpression significantly promotes tumor growth and compromises oxaliplatin therapeutic effects in xenografts; (E and F) Assessment of Oxaliplatin tumor suppression efficiency in KRAS-mutated CRC tumors. KLF5 overexpression promoted Oxaliplatin resistance, while KLF5 knockdown synergistically enhanced tumor growth inhibition when combined with Oxaliplatin treatment; (G and H) IHC staining was performed to evaluate CRC tumor cell proliferation (Ki-67) and apoptosis levels (TUNEL). KLF5 overexpression significantly promoted CRC cell proliferation and suppressed oxaliplatin-induced apoptosis in CRC cells. Data represent the mean ± SD, Student’s t-test. ^*P < 0.05; ^**P < 0.01; ^***P < 0.001. KLF5: Krüppel-like factor 5; CRC: colorectal cancer; SEM: standard error of the mean; IHC: immunohistochemistry; Ki-67: antigen Ki-67; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; SD: standard deviation.