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. 2010 Sep;177(3):1503–1513. doi: 10.2353/ajpath.2010.090651

Figure 1.

Figure 1

KLF5 regulates anchorage-independent growth of human lung cancer cells. A549, H441, H23, and H460 cells were stably transduced with KLF5 overexpression retrovirus (KLF5oe) or empty vector control virus (vector). A: Western analysis of KLF5 in protein lysates generated from nuclear extracts of KLF5 overexpressing or empty vector control A549 cells. Detection of TATA-binding protein (TBP) serves as loading control. KLF5 band intensities are reported as fold change relative to empty vector control. B: Representative images of KLF5 overexpressing or empty vector control H441 cells plated at high density that have reached confluence (Day 1) or three days later (Day 4). C: Average number of colonies formed in soft agar by A549, H441, H23, and H460 KLF5 overexpressing or empty vector control cells ± SEM. *P < 0.05 and ***P < 0.0005 by t-test. A549, H441, H23, and H460 cells were stably transduced with three different KLF5-specific shRNA lentiviruses (A–C) or nontargeting shRNA lentivirus control (NT). D: Western analysis of KLF5 expression in protein lysates generated from nuclear extracts of KLF5 knockdown or control A549 cells. TATA-binding protein serves as loading control. KLF5 band intensities are reported as fold change relative to nontargeting shRNA control. E: Average number of colonies formed in soft agar by A549, H441, H23, and H460 KLF5 knockdown or control cells ± SEM. **P < 0.005 and ***P < 0.0005 by t-test.