It is estimated that
breast cancer will be the second leading cause of
cancer-associated mortality in women in 2018. Previous research has demonstrated that the
atypical protein kinase C-ζ (PKC-ζ) is a component of numerous dysregulated pathways in
breast cancer, including cellular proliferation, survival, and cell cycle upregulation. The present study investigated the PKC-ζ
protein in breast tissue to evaluate its potential as a
biomarker for
breast cancer invasion, and demonstrated that an overexpression of PKC-ζ
protein can be indicative of
carcinogenesis. The present study analyzed the expression of PKC-ζ in individuals with no
tumor complications and malignant female human breast tissue samples (
lobular carcinoma in situ, invasive
lobular carcinoma,
ductal carcinoma in situ and invasive
ductal carcinoma) with the use of western blot analysis, immunohistochemistry and statistical analysis (83 samples). The present study also evaluated the invasive behavior of MDA-MB-231
breast cancer cells following the knockdown of PKC-ζ with a Transwell invasion assay and an immunofluorescent probe for filamentous actin (
F-actin) organization. The data demonstrated that PKC-ζ expression was identified to be higher in invading tissues when compared with non-invading tissues. The results also suggest that PKC-ζ is more abundant in ductal tissues when compared with lobular tissues. In addition, the
protein studies also suggest that PKC-ζ is a component for invasive behavior through the
Ras-related C3 botulinum toxin substrate 1 (Rac1) and Ras homolog gene family member A (RhoA) pathway, and PKC-ζ is required for the
F-actin reorganization in invasive cells. Therefore, PKC-ζ should be considered to be a
biomarker in the development of
breast cancer as well as an
indicator of invading
tumor cells.