Involvement of Plectin in the hemidesmosomes-deficient prostate cancer PC3 cells

Loss of a6ß4-dependent hemidesmosomes has been observed during prostate cancer progression. However, the significance and underlying mechanisms by which aberrant hemidesmosome assembly may modulate tumorigenesis remain elusive. Using RNAseq analysis we found that the most enriched pathways in hemidesmosomes-deficient PC3 cells were related to proliferation and cell cycle regulation and all the most affected pathways were upregulated in plectin-dependent manner.