scholarly journals HMGB1: A Promising Therapeutic Target for Prostate Cancer

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Munirathinam Gnanasekar ◽  
Ramaswamy Kalyanasundaram ◽  
Guoxing Zheng ◽  
Aoshuang Chen ◽  
Maarten C. Bosland ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
High Mobility ◽  
Chromatin Binding ◽  
Oncogenic Signaling ◽  
Prostate Cancer Treatment ◽  
Promising Therapeutic Target ◽  
Prostate Cancer Development ◽  
Oncogenic Signaling Pathways

High mobility group box 1 (HMGB1) was originally discovered as a chromatin-binding protein several decades ago. It is now increasingly evident that HMGB1 plays a major role in several disease conditions such as atherosclerosis, diabetes, arthritis, sepsis, and cancer. It is intriguing how deregulation of HMGB1 can result in a myriad of disease conditions. Interestingly, HMGB1 is involved in cell proliferation, angiogenesis, and metastasis during cancer progression. Furthermore, HMGB1 has been demonstrated to exert intracellular and extracellular functions, activating key oncogenic signaling pathways. This paper focuses on the role of HMGB1 in prostate cancer development and highlights the potential of HMGB1 to serve as a key target for prostate cancer treatment.

scholarly journals MZF1 and SCAND1 Reciprocally Regulate CDC37 Gene Expression in Prostate Cancer

Cancers ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 792 ◽  
Author(s):  
Takanori Eguchi ◽  
Thomas L. Prince ◽  
Manh Tien Tran ◽  
Chiharu Sogawa ◽  
Benjamin J. Lang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Heat Shock Protein 90 ◽  
Prostate Cancer Cells ◽  
Oncogenic Signaling ◽  
Normal Prostate ◽  
Elevated Expression ◽  
The Stability ◽  
Oncogenic Signaling Pathways

Cell division control 37 (CDC37) increases the stability of heat shock protein 90 (HSP90) client proteins and is thus essential for numerous intracellular oncogenic signaling pathways, playing a key role in prostate oncogenesis. Notably, elevated expression of CDC37 was found in prostate cancer cells, although the regulatory mechanisms through which CDC37 expression becomes increased are unknown. Here we show both positive and negative regulation of CDC37 gene transcription by two members of the SREZBP-CTfin51-AW1-Number 18 cDNA (SCAN) transcription factor family—MZF1 and SCAND1, respectively. Consensus DNA-binding motifs for myeloid zinc finger 1 (MZF1/ZSCAN6) were abundant in the CDC37 promoter region. MZF1 became bound to these regulatory sites and trans-activated the CDC37 gene whereas MZF1 depletion decreased CDC37 transcription and reduced the tumorigenesis of prostate cancer cells. On the other hand, SCAND1, a zinc fingerless SCAN box protein that potentially inhibits MZF1, accumulated at MZF1-binding sites in the CDC37 gene, negatively regulated the CDC37 gene and inhibited tumorigenesis. SCAND1 was abundantly expressed in normal prostate cells but was reduced in prostate cancer cells, suggesting a potential tumor suppressor role of SCAND1 in prostate cancer. These findings indicate that CDC37, a crucial protein in prostate cancer progression, is regulated reciprocally by MZF1 and SCAND1.

scholarly journals SCAND1 Suppresses CDC37 Gene Transcription by Repressing MZF1

2019 ◽  
Author(s):  
Takanori Eguchi ◽  
Thomas L. Prince ◽  
Tien Manh Tran ◽  
Chiharu Sogawa ◽  
Benjamin J. Lang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Gene Transcription ◽  
Cancer Progression ◽  
Prostate Cancer Cells ◽  
Oncogenic Signaling ◽  
Normal Prostate ◽  
Elevated Expression ◽  
The Stability ◽  
Oncogenic Signaling Pathways

Cell division control 37 (CDC37) increases the stability of HSP90 client proteins and is thus essential for numerous intracellular oncogenic signaling pathways, playing a key role in prostate oncogenesis. Notably, elevated expression of CDC37 was found in prostate cancer cells, although the regulatory mechanisms through which CDC37 expression becomes increased are unknown. Here we show both positive and negative regulation of CDC37 gene transcription by two members of the SCAN transcription factor family- MZF1 and SCAND1, respectively. Consensus DNA-binding motifs for myeloid zinc finger 1 (MZF1 / ZSCAN6) were abundant in the CDC37 promoter region. MZF1 became bound to these regulatory sites and trans-activated the CDC37 gene whereas MZF1 depletion decreased CDC37 transcription and reduced tumorigenesis of prostate cancer cells. On the other hand, SCAND1, a zinc-fingerless SCAN box protein that potentially inhibits MZF1, accumulated at MZF1-binding sites in CDC37 gene, negatively regulated CDC37 gene and inhibited tumorigenesis. SCAND1 was abundantly expressed in normal prostate cells but was reduced in prostate cancer cells, suggesting a potential tumor suppressor role of SCAND1 in prostate cancer. These findings indicate that CDC37, a crucial protein in prostate cancer progression, is regulated reciprocally by MZF1 and SCAND1.

scholarly journals SCAND1 suppresses CDC37 gene transcription by repressing MZF1

2019 ◽  
Author(s):  
Takanori Eguchi ◽  
Thomas L. Prince ◽  
Manh Tien Tran ◽  
Chiharu Sogawa ◽  
Benjamin J. Lang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Cells ◽  
Gene Transcription ◽  
Cancer Progression ◽  
Prostate Cancer Cells ◽  
Oncogenic Signaling ◽  
Normal Prostate ◽  
Elevated Expression ◽  
The Stability ◽  
Oncogenic Signaling Pathways

AbstractCDC37 increases the stability of HSP90 client proteins and is essential for numerous intracellular oncogenic signaling pathways. Elevated expression of CDC37 was found in prostate cancer cells, although the regulatory mechanisms through which CDC37 expression becomes increased are unknown. Here we show both positive and negative regulation of CDC37 gene transcription by two members of the SCAN transcription factor family- MZF1 and SCAND1, respectively. Consensus DNA-binding motifs for MZF1 were abundant in the CDC37 promoter region. MZF1 became bound to these regulatory sites and trans-activated the CDC37 gene whereas MZF1 depletion decreased CDC37 transcrption and reduced tumorigenesis of prostate cancer cells. On the other hand, SCAND1, a zinc-fingerless SCAN box protein that potentially inhibits MZF1, accumulated at MZF1-binding sites in CDC37 gene, negatively regulated CDC37 gene and inhibited tumorigenesis. SCAND1 was abundantly expressed in normal prostate cells but was reduced in prostate cancer cells, suggesting a potential tumor suppressor role of SCAND1 in prostate cancer. These findings indicate that CDC37, a crucial protein in prostate cancer progression, is regulated reciprocally by MZF1 and SCAND1.

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