fig5

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

Figure 5. KLF5 drives proliferation and cell cycle progression in KRAS-mutated CRC via upregulation of the CDK4/6-Cyclin D1 axis. (A) RNA-seq analysis of differentially expressed cell cycle-related genes in KLF5-knockdown KRAS-mutant CRC cells; (B and C) Western blot analysis of KLF5, cell cycle regulators (CDK1, CDK2, CDK4, CDK6, Cyclin D1, Cyclin D2, Cyclin E1), and cell cycle inhibitors (p21, p16) in KRAS-mutant CRC cells, with GAPDH as a loading control. 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; CDK: cyclin-dependent kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; SD: standard deviation.