Next Article in Journal
Digital Droplet PCR is a Specific and Sensitive Tool for Detecting IDH2 Mutations in Acute Myeloid LeuKemia Patients
Next Article in Special Issue
Immunotherapy in Prostate Cancer
Previous Article in Journal
Calcium Signaling Alterations Caused by Epigenetic Mechanisms in Pancreatic Cancer: From Early Markers to Prognostic Impact
Previous Article in Special Issue
PSMA Theranostics: Review of the Current Status of PSMA-Targeted Imaging and Radioligand Therapy
Open AccessArticle

SETD1A Promotes Proliferation of Castration-Resistant Prostate Cancer Cells via FOXM1 Transcription

Gachon Research Institute of Pharmaceutical Sciences, College of Pharmacy, Gachon University, 191 Hambakmoero, Yeonsu-gu, Incheon 21936, Korea
*
Author to whom correspondence should be addressed.
Cancers 2020, 12(7), 1736; https://doi.org/10.3390/cancers12071736
Received: 20 May 2020 / Revised: 17 June 2020 / Accepted: 26 June 2020 / Published: 30 June 2020
(This article belongs to the Special Issue New Therapies for Prostate Cancer)
Androgen deprivation therapy eventually leads to the development of castration-resistant prostate cancer (CRPC). Here, we demonstrate for the first time that the histone H3K4 methyltransferase SETD1A is a major regulator for the proliferation of metastatic CRPC (mCRPC). The expression of SETD1A was significantly correlated with the survival rate of patients with prostate cancer. SETD1A, which is expressed at a higher level in mCRPC than in primary prostate cancer cells, promotes the expression of FOXM1, a gene encoding a cell proliferation-specific transcription factor. SETD1A is recruited to the promoter region of FOXM1 (forkhead box M1) upon binding to E2F1, a protein that regulates the transcription of FOXM1 and contributes to the trimethylation of H3K4 in the FOXM1 promoter region. In addition, SETD1A is essential for the expression of stem cell factor (e.g., OCT4, octamer-binding transcription factor 4) and stem cell formation in mCRPC, suggesting the importance of SETD1A expression in mCRPC tumor formation. Notably, poor prognosis is associated with high expression of the SETD1A–FOXM1 pair in clinical data sets. Therefore, our study suggests that SETD1A plays an important role in the proliferation of mCRPC by regulating FOXM1 transcription. View Full-Text
Keywords: SETD1A; FOXM1; prostate cancer; castration-resistant SETD1A; FOXM1; prostate cancer; castration-resistant
Show Figures

Figure 1

MDPI and ACS Style

Yang, L.; Jin, M.; Park, S.J.; Seo, S.-Y.; Jeong, K.W. SETD1A Promotes Proliferation of Castration-Resistant Prostate Cancer Cells via FOXM1 Transcription. Cancers 2020, 12, 1736.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop