Stabilization of the prostate-specific tumor suppressor NKX3.1 by the oncogenic protein kinase Pim-1 in prostate cancer cells

2013 ◽  
Vol 114 (5) ◽  
pp. 1050-1057 ◽  
Author(s):  
Achuth Padmanabhan ◽  
Eliza B. Gosc ◽  
Charles J. Bieberich
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Specific Tumor ◽  
Oncogenic Protein

scholarly journals Crosstalk between Prostate Cancer Cells and Tumor-Associated Fibroblasts Enhances the Malignancy by Inhibiting the Tumor Suppressor PLZF

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1083
Author(s):  
Kum Hee Noh ◽  
Ae Jin Jeong ◽  
Haeri Lee ◽  
Song-Hee Lee ◽  
Eunhee Yi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Suppressor ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Metastasis ◽  
Tyrosine Phosphatase ◽  
Migration And Invasion ◽  
Metastatic Progression ◽  
Prostate Cancer Cells ◽  
Prostate Cancer Metastasis

Although prostate cancer is clinically manageable during the early stages of progression, metastatic progression severely compromises the prognosis and leads to mortality. Constitutive activation of STAT3 has been connected to prostate cancer malignancy, and abolishing the STAT3 activity may diminish tumor growth and metastasis. However, its suppressor genes and pathways have not been well established. In this study, we show that promyelocytic leukemia zinc finger (PLZF) has a putative tumor-suppressor function in prostate cancer by inhibiting phosphorylation of STAT3. Compared with a benign prostate, high-grade prostate cancer patient tissue was negatively correlated with PLZF expression. PLZF depletion accelerated proliferation and survival, migration, and invasion in human prostate cancer cells. Mechanistically, we demonstrated a novel role of PLZF as the transcriptional regulator of the tyrosine phosphatase SHP-1 that inhibits the oncogenic JAKs–STAT3 pathway. These results suggest that the collapse of PLZF expression by the CCL3 derived from fibroblasts accelerates the cell migration and invasion properties of prostate cancer cells. Our results suggest that increasing PLZF could be an attractive strategy for suppressing prostate cancer metastasis as well as for tumor growth.

scholarly journals Protein kinase Cɛ interacts with Bax and promotes survival of human prostate cancer cells

Oncogene ◽  
2003 ◽  
Vol 22 (39) ◽  
pp. 7958-7968 ◽  
Author(s):  
Meagan A McJilton ◽  
C Van Sikes ◽  
Ginger G Wescott ◽  
Daqing Wu ◽  
Tonia L Foreman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Prostate Cancer Cells
Sign in / Sign up

Export Citation Format

Share Document