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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Kim, Soyoung Chun, So-Young Kwon, Yun-Suk Nam, Kyung-Soo |
| Description | Author Affiliation: Kim S ( Department of Pharmacology, School of Medicine and Intractable Disease Research Center, Dongguk University, 123 Dongdae-ro, Gyeongju-si, Gyeongsangbuk-do 38066, Republic of Korea.); Chun SY ( Department of Pharmacology, School of Medicine and Intractable Disease Research Center, Dongguk University, 123 Dongdae-ro, Gyeongju-si, Gyeongsangbuk-do 38066, Republic of Korea.); Kwon YS ( Department of Pharmacology, School of Medicine and Intractable Disease Research Center, Dongguk University, 123 Dongdae-ro, Gyeongju-si, Gyeongsangbuk-do 38066, Republic of Korea.); Nam KS ( Department of Pharmacology, School of Medicine and Intractable Disease Research Center, Dongguk University, 123 Dongdae-ro, Gyeongju-si, Gyeongsangbuk-do 38066, Republic of Korea. Electronic address: namks@dongguk.ac.kr.) |
| Abstract | Although many studies have implicated the crosstalk between the Wnt and PKC signaling pathways in tumor initiation and progression, the molecular roles of PKC isoforms in the Wnt signaling pathway remain poorly understood. In this study, we explored the contribution of PKC isoforms to canonical and noncanonical Wnt signaling pathway in mediating cell migration and an epithelial-mesenchymal transition (EMT). When MCF-7 cells were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) for up to 3 weeks, the effect of TPA on Wnt signaling pathway was dramatically different depending on the exposure time. The short term exposure (3 days) of MCF-7 cells to TPA exhibited significant induction of Wnt5a expression, along with the enhanced expression of PKC- , to promote cell migration, which suggested that activation of noncanonical Wnt signaling pathway is associated with PKC- . However, the chronic exposure (3 weeks) of cells to TPA completely suppressed Wnt5a expression and the expression of PKC-η and PKC-δ, whereas the expression of Wnt3a and PKC-θ were up-regulated to activate the canonical Wnt signaling pathway. Moreover, the loss of epithelial markers, including E-cadherin and GATA-3, suggested that chronic exposure of TPA stimulates EMT. Taken together, our data suggest that PKC-θ positively regulates the canonical Wnt signaling pathway, and that PKC-η and PKC-δ negatively modulate this signaling pathway. |
| File Format | HTM / HTML |
| ISSN | 07533322 |
| Volume Number | 77 |
| e-ISSN | 19506007 |
| Journal | Biomedicine & Pharmacotherapy |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2016-02-01 |
| Publisher Place | France |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Pharmacology Breast Neoplasms Genetics Protein Kinase C Proto-oncogene Proteins Tetradecanoylphorbol Acetate Pharmacology Wnt Proteins Wnt Signaling Pathway Radiation Effects Cadherins Metabolism Cell Movement Epithelial-mesenchymal Transition Physiology Gata3 Transcription Factor Humans Mcf-7 Cells Protein Kinase C-alpha Time Factors Up-regulation Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Pharmacology |
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