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Characterization of glycine‐ N ‐acyltransferase like 1 (GLYATL1) in prostate cancer
Author(s) -
Eich MarieLisa,
Chandrashekar Darshan Shimoga,
Rodriguez Pen᷉a Maria Del Carmen,
Robinson Alyncia D.,
Siddiqui Javed,
DaignaultNewton Stephanie,
Chakravarthi Balabhadrapatruni V. S. K.,
Kunju Lakshmi Priya,
Netto George J.,
Varambally Sooryanarayana
Publication year - 2019
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.23887
Subject(s) - prostate cancer , lncap , prostate , cancer research , gene knockdown , pca3 , transcriptome , cancer , biology , medicine , gene expression , gene , genetics
Background Recent microarray and sequencing studies of prostate cancer showed multiple molecular alterations during cancer progression. It is critical to evaluate these molecular changes to identify new biomarkers and targets. We performed analysis of glycine‐ N ‐acyltransferase like 1 (GLYATL1) expression in various stages of prostate cancer in this study and evaluated the regulation of GLYATL1 by androgen. Method We performed in silico analysis of cancer gene expression profiling and transcriptome sequencing to evaluate GLYATL1 expression in prostate cancer. Furthermore, we performed immunohistochemistry using specific GLYATL1 antibody using high‐density prostate cancer tissue microarray containing primary and metastatic prostate cancer. We also tested the regulation of GLYATL1 expression by androgen and ETS transcription factor ETV1. In addition, we performed RNA‐sequencing of GLYATL1 modulated prostate cancer cells to evaluate the gene expression and changes in molecular pathways. Results Our in silico analysis of cancer gene expression profiling and transcriptome sequencing we revealed an overexpression of GLYATL1 in primary prostate cancer. Confirming these findings by immunohistochemistry, we show that GLYATL1 is overexpressed in primary prostate cancer compared with metastatic prostate cancer and benign prostatic tissue. Low‐grade cancers had higher GLYATL1 expression compared to high‐grade prostate tumors. Our studies showed that GLYATL1 is upregulated upon androgen treatment in LNCaP prostate cancer cells which harbors ETV1 gene rearrangement. Furthermore, ETV1 knockdown in LNCaP cells showed downregulation of GLYATL1 suggesting potential regulation of GLYATL1 by ETS transcription factor ETV1. Transcriptome sequencing using the GLYATL1 knockdown prostate cancer cell lines LNCaP showed regulation of multiple metabolic pathways. Conclusions In summary, our study characterizes the expression of GLYATL1 in prostate cancer and explores the regulation of its regulation in prostate cancer showing role for androgen and ETS transcription factor ETV1. Future studies are needed to decipher the biological significance of these findings.