Document Type


Publication Date


Digital Object Identifier (DOI)


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.

Rights Information

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Was this content written or created while at USF?


Citation / Publisher Attribution

Oncology Letters, v. 17, issue 2, p. 1537-1546