Differential gene expression of BCL-2, ZEB2-AS1 and BALR-2 in prostate cancer and benign prostatic hyperplasia.
LncRNA
apoptosis
benign prostate hyperplasia
prostate cancer
Journal
Andrologia
ISSN: 1439-0272
Titre abrégé: Andrologia
Pays: Germany
ID NLM: 0423506
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
revised:
15
11
2021
received:
01
07
2021
accepted:
27
11
2021
pubmed:
7
12
2021
medline:
11
3
2022
entrez:
6
12
2021
Statut:
ppublish
Résumé
Prostate cancer (PCa) and benign prostate hyperplasia (BPH) are highly prevalent heterogeneous disorders among men. Whereas PCa and BPH underline common pathological features, apoptotic-related genes might be differentially expressed in these diseases. This study was aimed at testing BCL-2 as well as BALR-2 and ZEB2-AS1 apoptosis-related long non-coding RNA (lncRNA) in patients with PCa and BPH. The expression levels of the BCL-2 gene and ZEB2-AS1 lncRNA were upregulated in tumoural tissues in comparison to adjacent non-cancerous tissues (ANCTs) and BPH tissues. In contrast, the expression level of BALR-2 lncRNA was significantly higher in BPH compared with tumoural tissues. Furthermore, while no association was noticed between the relative expression of ZEB2-AS1 and the tumour grade, the relative expression of BCL-2 and BALR-2 is strongly associated with a higher grade of the tumour in PCa samples compared with the ANCTs. The receiver operating characteristic (ROC) curve analysis indicated the highest specificity and diagnostic value in distinguishing PCa and ANCTs as well as PCa and BPH, respectively. In conclusion, altered expression of BCL-2 and BALR-2 was observed to be associated with tumoural progression and could be used as potential candidates for distinguishing PCa tissues from ANCTs or BPH samples.
Substances chimiques
BCL2 protein, human
0
Proto-Oncogene Proteins c-bcl-2
0
RNA, Long Noncoding
0
Zinc Finger E-box Binding Homeobox 2
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e14344Informations de copyright
© 2021 Wiley-VCH GmbH.
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