fig1

KLF5 promotes tumor proliferation and oxaliplatin resistance via chromatin remodeling in KRAS-mutated colorectal cancer

Figure 1. KRAS-mutant CRC exhibits elevated KLF5 expression, enhanced proliferation, and reduced sensitivity to oxaliplatin compared to KRAS wild-type CRC. (A) Oxaliplatin treatment in KRAS wild-type CRC; (B) Oxaliplatin treatment in KRAS-mutant CRC; (C and D) Dose-response curves demonstrating decreased oxaliplatin sensitivity in KRAS-mutant CRC, with significantly higher IC50 values compared to KRAS wild-type CRC; (E) Growth status of CRC PDOs, showing enhanced proliferative capacity in KRAS-mutant CRC PDOs; (F-H) Representative IHC staining images from a tissue microarray containing 75 paired CRC and adjacent N tissues. KLF5 expression shows no significant difference between T and adjacent N tissues, but is significantly upregulated in KRAS-mutant CRC; (I and J) qPCR analysis of KLF5 RNA expression levels in 18 paired CRC and adjacent N tissues. KLF5 mRNA expression shows no significant difference between T and adjacent N tissues, but is significantly upregulated in KRAS-mutant CRC; (K) KLF5 expression profiles in CRC cell lines. Data represent the mean ± SD, Student’s t-test. *P < 0.05; **P < 0.01; ***P <  0.001. CRC: Colorectal cancer; KLF5: Krüppel-like factor 5; IC50: half maximal inhibitory concentration; PDOs: patient-derived organoids; IHC: immunohistochemistry; qPCR: quantitative polymerase chain reaction; RNA: ribonucleic acid; mRNA: messenger RNA; SD: standard deviation; T: tumor; N: normal.

Cancer Drug Resistance
ISSN 2578-532X (Online)

Portico

All published articles will preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles will preserved here permanently:

https://www.portico.org/publishers/oae/