KLF9, a transcription factor induced in flutamide-caused cell apoptosis, inhibits AKT activation and suppresses tumor growth of prostate cancer cells

The Prostate ◽  
2014 ◽  
Vol 74 (9) ◽  
pp. 946-958 ◽  
Author(s):  
Pengliang Shen ◽  
Jiabin Sun ◽  
Guiqin Xu ◽  
Li Zhang ◽  
Zhaojuan Yang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Prostate Cancer Cells ◽  
Akt Activation

scholarly journals An Anti-PSMA Immunotoxin Reduces Mcl-1 and Bcl2A1 and Specifically Induces in Combination with the BAD-Like BH3 Mimetic ABT-737 Apoptosis in Prostate Cancer Cells

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1648
Author(s):  
Anie P. Masilamani ◽  
Viviane Dettmer-Monaco ◽  
Gianni Monaco ◽  
Toni Cathomen ◽  
Irina Kuckuck ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Combination Therapy ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Xenograft Model ◽  
Target Cells ◽  
Prostate Cancer Cells ◽  
Mouse Xenograft Model ◽  
Synergistic Cytotoxicity ◽  
3D Spheroids

Background: Upregulation of anti-apoptotic Bcl-2 proteins in advanced prostate cancer leads to therapeutic resistance by prevention of cell death. New therapeutic approaches aim to target the Bcl-2 proteins for the restoration of apoptosis. Methods: The immunotoxin hD7-1(VL-VH)-PE40 specifically binds to the prostate specific membrane antigen (PSMA) on prostate cancer cells and inhibits protein biosynthesis. It was tested with respect to its effects on the expression of anti-apoptotic Bcl-2 proteins. Combination with the BAD-like mimetic ABT-737 was examined on prostate cancer cells and 3D spheroids and in view of tumor growth and survival in the prostate cancer SCID mouse xenograft model. Results: The immunotoxin led to a specific inhibition of Mcl-1 and Bcl2A1 expression in PSMA expressing target cells. Its combination with ABT-737, which inhibits Bcl-2, Bcl-xl, and Bcl-w, led to an induction of the intrinsic apoptotic pathway and to a synergistic cytotoxicity in prostate cancer cells and 3D spheroids. Furthermore, combination therapy led to a significantly prolonged survival of mice bearing prostate cancer xenografts based on an inhibition of tumor growth. Conclusion: The combination therapy of anti-PSMA immunotoxin plus ABT-737 represents the first tumor-specific therapeutic approach on the level of Bcl-2 proteins for the induction of apoptosis in prostate cancer.

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.

Klf4 transcription factor is expressed in the cytoplasm of prostate cancer cells

2013 ◽  
Vol 49 (4) ◽  
pp. 955-963 ◽  
Author(s):  
Clémentine Le Magnen ◽  
Lukas Bubendorf ◽  
Christian Ruiz ◽  
Inti Zlobec ◽  
Alexander Bachmann ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Prostate Cancer Cells

Abstract 4395: The cMYC-associated transcription factor JPO2 is upregulated in taxane resistant prostate cancer cells and interacts with the stress oncoprotein LEDGF/p75

2019 ◽  
Author(s):  
Greisha L. Ortiz Hernandez ◽  
Shannalee Martinez ◽  
Evelyn Sanchez-Hernandez ◽  
Leslimar Rios-Colon ◽  
Christina Cajigas-DuRoss ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Prostate Cancer Cells
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