A Novel Androgen-Induced lncRNA FAM83H-AS1 Promotes Prostate Cancer Progression via the miR-15a/CCNE2 Axis

Prostate cancer (PCa) is one of the most common types of tumors among males worldwide. However, the roles of long noncoding RNAs (lncRNAs) in PCa remain unclear. This study shows that lncRNA FAM83H-AS1 is upregulated in prostate adenocarcinoma, bladder urothelial carcinoma, and kidney renal papillary cell carcinoma samples. Androgen receptor (AR) signaling plays the most important role in PCa tumorigenesis and development. In this study, the results validate that AR signaling is involved in upregulating FAM83H-AS1 expression in PCa cells. Loss-of-function assays demonstrate that FAM83H-AS1 acts as an oncogene in PCa by modulating cell proliferation, cell cycle, and migration. Bioinformatics analysis demonstrates that FAM83H-AS1 is remarkably related to the regulation of the cell cycle and DNA replication through affecting multiple regulators related to these pathways, such as CCNE2. Mechanically, we found that FAM83H-AS1 plays its roles through sponging miR-15a to promote CCNE2 expression. These findings indicate that FAM83H-AS1 is a novel diagnostic and therapeutic marker for PCa.

Download Full-text

Abstract 5238: Integrative analysis of functional long noncoding RNAs during prostate cancer progression

10.1158/1538-7445.am2014-5238 ◽

2014 ◽

Author(s):

Teng Fei ◽

Yiwen Chen ◽

Zhou Du ◽

Xiaole Shirley Liu ◽

Myles Brown

Keyword(s):

Prostate Cancer ◽

Cancer Progression ◽

Noncoding Rnas ◽

Integrative Analysis ◽

Long Noncoding Rnas ◽

Prostate Cancer Progression

Download Full-text

Prostate Cancer Progression: Aspirin Causes Cell Cycle Quiescence in Prostate Cancer Cells

International Journal of Surgery ◽

10.1016/j.ijsu.2018.05.725 ◽

2018 ◽

Vol 55 ◽

pp. S11-S12 ◽

Cited By ~ 1

Author(s):

P. Oluseyi Olalekan Olaniyi ◽

H. Whiteland ◽

U.K. Shah ◽

O. Bodger ◽

J. Verma ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Cycle ◽

Cancer Cells ◽

Cancer Progression ◽

Prostate Cancer Progression ◽

Prostate Cancer Cells

Download Full-text

KLF6 Loss of Function in Human Prostate Cancer Progression Is Implicated in Resistance to Androgen Deprivation

American Journal Of Pathology ◽

10.1016/j.ajpath.2012.06.008 ◽

2012 ◽

Vol 181 (3) ◽

pp. 1007-1016 ◽

Cited By ~ 17

Author(s):

XiaoMei Liu ◽

Alejandro Gomez-Pinillos ◽

Charisse Loder ◽

Enrique Carrillo-de Santa Pau ◽

Ruifang Qiao ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Progression ◽

Androgen Deprivation ◽

Human Prostate ◽

Human Prostate Cancer ◽

Prostate Cancer Progression ◽

Loss Of Function

Download Full-text

Quantitative Proteomics of TRAMP Mice Combined with Bioinformatics Analysis Reveals That PDGF-B Regulatory Network Plays a Key Role in Prostate Cancer Progression

Journal of Proteome Research ◽

10.1021/acs.jproteome.8b00158 ◽

2018 ◽

Vol 17 (7) ◽

pp. 2401-2411 ◽

Cited By ~ 5

Author(s):

Yuan Zhang ◽

Dan Wang ◽

Min Li ◽

Xiaodan Wei ◽

Shuang Liu ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Progression ◽

Regulatory Network ◽

Quantitative Proteomics ◽

Bioinformatics Analysis ◽

Prostate Cancer Progression ◽

Tramp Mice

Download Full-text

YY1 cistrome analysis uncovers an essential requirement of the YY1:BRD4-PFKP regulatory axis for promoting tumorigenesis of castration-resistant prostate cancer

10.1101/2020.09.17.302596 ◽

2020 ◽

Author(s):

Chenxi Xu ◽

Yi-Hsuan Tsai ◽

Phillip Galbo ◽

Weida Gong ◽

Aaron J. Storey ◽

...

Keyword(s):

Prostate Cancer ◽

Tumor Cell ◽

Cancer Progression ◽

Advanced Prostate Cancer ◽

Regulatory Element ◽

Prostate Cancer Progression ◽

Castration Resistant Prostate Cancer ◽

Loss Of Function ◽

Master Regulator ◽

Castration Resistant

AbstractCastration-resistant prostate cancer (CRPC) is a terminal disease, demanding a better understanding of its pathogenesis. Targeted therapy needs to be developed for CRPC due to its heterogeneity and resistance to current treatments. Here, through cistrome study of YY1, a transcription factor significantly overexpressed during prostate cancer progression, we identify a YY1-PFKP axis to be essential for CRPC tumorigenesis. Depletion of YY1 in independent CRPC models dramatically reduced tumor cell growth in vitro and delayed oncogenic progression in vivo. Importantly, YY1 functions as a master regulator of prostate tumor metabolism including the Warburg effect and mitochondria respiration. Loss-of-function and rescue studies further reveals a mechanistic underpinning in which YY1 directly binds and trans-activates PFKP, a gene encoding the rate-limiting enzyme for glycolysis, significantly contributing to the YY1-enforced oncogenic phenotypes such as enhanced tumor cell glycolysis and malignant growth. Additionally, a vast majority of gene-regulatory element in advanced prostate cancer cells are bound by YY1, lending a support for its role as a master regulator of prostate cancer progression. YY1 interactome studies point to bromodomain-containing coactivators in prostate cancer, which act as functional partners of YY1 to potentiate YY1-related target gene activation. Altogether, this study unveils an unexplored YY1:BRD4-PFKP oncogenic axis operating in advanced prostate cancer with implications for therapy.

Download Full-text