scholarly journals Role of splice variants in the metastatic progression of prostate cancer

2012 ◽  
Vol 40 (4) ◽  
pp. 870-874 ◽  
Author(s):  
Rachel M. Hagen ◽  
Michael R. Ladomery

AS (alternative splicing) and its role in disease, especially cancer, has come to forefront in research over the last few years. Alterations in the ratio of splice variants have been widely observed in cancer. Splice variants of cancer-associated genes have functions that can alter cellular phenotype, ultimately altering metastatic potential. As metastases are the cause of approximately 90% of all human cancer deaths, it is crucial to understand how AS is dysregulated in metastatic disease. We highlight some recent studies into the relationship between altered AS of key genes and the initiation of prostate cancer metastasis.

2018 ◽  
Vol Volume 10 ◽  
pp. 4029-4038 ◽  
Author(s):  
Fei Zhan ◽  
Jingling Shen ◽  
Ruitao Wang ◽  
Liang Wang ◽  
Yao Dai ◽  
...  

2008 ◽  
Vol 7 (11) ◽  
pp. 1849-1851 ◽  
Author(s):  
Candece L. Gladson ◽  
Danny R. Welch

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1083
Author(s):  
Kum Hee Noh ◽  
Ae Jin Jeong ◽  
Haeri Lee ◽  
Song-Hee Lee ◽  
Eunhee Yi ◽  
...  

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.


2020 ◽  
Vol Volume 13 ◽  
pp. 7411-7422 ◽  
Author(s):  
Lin Tang ◽  
Meng Xu ◽  
Long Zhang ◽  
Lin Qu ◽  
Xiaoyan Liu

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