J Cancer 2017; 8(15):3028-3036. doi:10.7150/jca.20467 This issue
1. Bachelor Program of Senior Services, Southern Taiwan University of Science and Technology, Tainan, Taiwan;
2. Institute of Biochemistry and Biotechnology, Medical College, Chung-Shan Medical University, Taichung, Taiwan;
3. Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan;
4. Department Physical Therapy, School of Medical and Health Sciences, Fooyin University, Kaohsiung, Taiwan;
5. Institute of Nutrition, College of Biopharmaceutical and Food Sciences, China Medical University, Taichung, Taiwan;
6. Department of Medical Applied Chemistry, College of Health Care and Management, Chung Shan Medical University, Taichung, Taiwan;
7. Department of Medical Research, Tungs' Taichung MetroHarbor Hospital, Taichung, Taiwan;
8. Center for Molecular Medicine, China Medical University Hospital, Taichung, Taiwan;
9. Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan.
Background: Protein kinase C alpha (PKCα) is a key signaling molecule in human cancer development. As a therapeutic strategy, targeting PKCα is difficult because the molecule is ubiquitously expressed in non-malignant cells. PKCα is regulated by the cooperative interaction of the transcription factors myeloid zinc finger 1 (MZF-1) and Ets-like protein-1 (Elk-1) in human cancer cells.
Methods: By conducting tissue array analysis, herein, we determined the protein expression of MZF-1/Elk-1/PKCα in various cancers.
Results: The data show that the expression of MZF-1/Elk-1 is correlated with that of PKCα in hepatocellular carcinoma (HCC), but not in bladder and lung cancers. In addition, the PKCα down-regulation by shRNA Elk-1 was only observed in the HCC SK-Hep-1 cells. Blocking the interaction between MZF-1 and Elk-1 through the transfection of their binding domain MZF-160-72 decreased PKCα expression. This step ultimately depressed the epithelial-mesenchymal transition potential of the HCC cells.
Conclusion: These findings could be used to develop an alternative therapeutic strategy against patients with the PKCα-derived HCC.
Keywords: MZF-1, Elk-1, PKCα, HCC.