Panoply™ Human CDH2 Knockdown Stable Cell Line

Here, researchers investigated the diagnostic, prognostic, and therapeutic value of cadherin family genes (CDH1, CDH2, and CDH3) in non-small cell lung cancer (NSCLC) subtypes: lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Results showed that expression of CDH1, CDH2, and CDH3 was significantly elevated in both LUAD and LUSC. Methylation analysis revealed decreased methylation of the cadherin gene promoters in tumor samples compared with normal tissue. Mutation analysis revealed that CDH2 had the highest mutation frequency (63%), followed by CDH3 (23%) and CDH1 (19%). Survival analysis demonstrated that elevated expression of CDH1, CDH2, and CDH3 was associated with poor prognosis in both LUAD and LUSC. Knockdown of CDH1 and CDH2 in PC9 cells impaired cell proliferation, colony formation, and wound healing, with CDH2 knockdown having a more pronounced effect. Thus, CDH1, CDH2, and CDH3 are upregulated in LUAD and LUSC, leading to tumor progression and poor prognosis. Knockdown of CDH1 and CDH2 in PC9 cells impairs cell proliferation, colony formation, and wound healing, highlighting their potential as therapeutic targets.

Here, researchers investigated the effects of CDH1 and CDH2 knockdown on various cellular processes in PC9 cells. Knockdown experiments revealed a significant decrease in CDH1 and CDH2 mRNA expression (Figure 1A). Western blot analysis confirmed this, showing a corresponding decrease in CDH1 and CDH2 protein levels in knockdown cells (Figure 1B). Furthermore, cell proliferation was significantly impaired in both CDH1 and CDH2 knockdown cells, with CDH2 knockdown leading to a more pronounced inhibition of proliferation (Figure 1C). Clonogenic assays demonstrated that both knockdowns reduced the number of colonies, with CDH2 knockdown cells showing a particularly low number of colonies formed (Figures 1D and 1E). Furthermore, wound healing assays revealed that both CDH1 and CDH2 knockdowns significantly impaired wound closure, with CDH2 knockdown resulting in the most severe delay (Figures 1F-H).

Figure 1. Knockdown effects of CDH1 and CDH2 on cell proliferation, colony formation, and wound healing in PC9 cells. (Wang Y, et al., 2025)