lncRNA PITPNA-AS1 promotes cell proliferation and metastasis in hepatocellular carcinoma by upregulating PDGFD.
Humans
Carcinoma, Hepatocellular
/ pathology
Liver Neoplasms
/ pathology
RNA, Long Noncoding
/ genetics
MicroRNAs
/ genetics
Cell Line, Tumor
Disease Progression
Cell Proliferation
/ genetics
Platelet-Derived Growth Factor
/ genetics
Gene Expression Regulation, Neoplastic
Cell Movement
/ genetics
Lymphokines
/ genetics
PDGFD
PITPNA-AS1
hepatocellular carcinoma
lncRNA
miR-363-5p
Journal
Aging
ISSN: 1945-4589
Titre abrégé: Aging (Albany NY)
Pays: United States
ID NLM: 101508617
Informations de publication
Date de publication:
02 03 2023
02 03 2023
Historique:
received:
10
10
2021
accepted:
11
02
2023
medline:
7
6
2023
pubmed:
31
5
2023
entrez:
30
5
2023
Statut:
ppublish
Résumé
Hepatocellular carcinoma (HCC) ranks high in morbidity and mortality among notorious malignancies because of the lack of effective biomarkers and treatments. LncRNA PITPNA antisense RNA 1 (PITPNA-AS1) plays an oncogenic role in HCC, yet the mechanistic basis remains unprobed. Here using Bioinformatics and PCR analyses, we validated that PITPNA-AS1 expression was significantly increased in HCC. The levels of PITPNA-AS1 in tumors were reversely correlated with the prognosis in HCC patients. Downregulation of PITPNA-AS1 inhibited malignant activities of HCC cells. Next, we elucidated that PITPNA-AS1 acts as a competing endogenous RNA (ceRNA) to sponge miR-363-5p, thereby regulating the expression of platelet-derived growth factor-D (PDGFD). Moreover, the suppression of HCC cell activities by PITPNA-AS1 downregulation can be removed by PDGFD overexpression or miR-363-5p inhibition. Collectively, our work reveals the involvement of the PITPNA-AS1/miR-363-5p/PDGFD regulatory axis in HCC progression.
Identifiants
pubmed: 37253627
pii: 204566
doi: 10.18632/aging.204566
pmc: PMC10258019
doi:
Substances chimiques
RNA, Long Noncoding
0
MicroRNAs
0
Platelet-Derived Growth Factor
0
PDGFD protein, human
0
Lymphokines
0
MIRN363 microRNA, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4071-4083Références
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