Expression of long non-coding RNA SFTA1P and its function in non-small cell lung cancer.
Adult
Aged
Aged, 80 and over
Carcinogenesis
/ genetics
Carcinoma, Non-Small-Cell Lung
/ genetics
Cell Line, Tumor
Cell Proliferation
/ genetics
Cell Transformation, Neoplastic
/ genetics
Gene Expression Regulation, Neoplastic
/ genetics
Humans
Lung Neoplasms
/ genetics
Middle Aged
Proto-Oncogene Proteins c-akt
/ metabolism
RNA, Long Noncoding
/ genetics
Cell cycle
Long non-coding RNA
Non-small cell lung cancer
PI3K-AKT signaling pathway
SFTA1P
Journal
Pathology, research and practice
ISSN: 1618-0631
Titre abrégé: Pathol Res Pract
Pays: Germany
ID NLM: 7806109
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
01
04
2020
revised:
23
05
2020
accepted:
05
06
2020
entrez:
23
8
2020
pubmed:
23
8
2020
medline:
2
7
2021
Statut:
ppublish
Résumé
Non-small cell lung cancer (NSCLC) is a major type of lung cancer with high morbidity and mortality. Long non-coding RNAs (lncRNAs) have been reported to be important in development and progression of NSCLC. However, the role of lncRNA SFTA1P remains unclear. This study aims to explore the clinical roles, biological function, and mechanism of SFTA1P in NSCLC. SFTA1P expression was estimated by the quantitative real-time polymerase chain reaction (qRT-PCR) of 90 pairs of tissue samples, the Cancer Genome Atlas (TCGA) database and microarray. After overexpressing SFTA1P, NSCLC cell proliferation, cycle, and apoptosis were detected. We found that the expression of SFTA1P was significantly downregulated in NSCLC tissues with high diagnostic value (AUC = 0.87), which was consistent with the results of TCGA and microarray data. For the analysis of clinical features, the results revealed that SFTA1P expression was closely related to the pathological type (P < 0.01). Furthermore, the cell function results suggested that the overexpression of SFTA1P triggered cell cycle arrest in the S-phase (P < 0.05). From a mechanistic perspective, the results showed that the PI3K-AKT signaling pathway was inhibited after overexpression of SFTA1P in NSCLC. Taken together, this work supported that SFTA1P may play a suppressing role in the tumorigenesis of NSCLC by modulating PI3K-AKT signaling pathway to influence cell cycle, which provides a potential and prospective biomarker for NSCLC.
Identifiants
pubmed: 32825934
pii: S0344-0338(20)30933-X
doi: 10.1016/j.prp.2020.153049
pii:
doi:
Substances chimiques
RNA, Long Noncoding
0
long non-coding RNA SFTA1P, human
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
153049Informations de copyright
Copyright © 2020 Elsevier GmbH. All rights reserved.