Upregulation of ADAMDEC1 correlates with tumor progression and predicts poor prognosis in non‐small cell lung cancer (NSCLC) via the PI3K/AKT pathway
Background ADAM‐like decysin‐1 (ADAMDEC1) has been reported to play an important role in the pathogenesis of multiple diseases, including cancers. However, its biological role in non‐small cell lung cancer (NSCLC) remains largely unknown. Here, we aimed to investigate the biological functions and po...
Gespeichert in:
Veröffentlicht in: | Thoracic cancer 2022-04, Vol.13 (7), p.1027-1039 |
---|---|
Hauptverfasser: | , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Background
ADAM‐like decysin‐1 (ADAMDEC1) has been reported to play an important role in the pathogenesis of multiple diseases, including cancers. However, its biological role in non‐small cell lung cancer (NSCLC) remains largely unknown. Here, we aimed to investigate the biological functions and potential mechanism of ADAMDEC1 in NSCLC.
Methods
We verified ADAMDEC1 as a DEG by a comprehensive strategy of TCGA and GEO datasets miming and computational biology. Relative levels of ADAMDEC1 in NSCLC tissues and the adjacent peritumoral tissues were identified by qRT‐PCR, WB and IHC staining. The biological function of ADAMDEC1 was determined by CCK8, EdU, colony formation assay, apoptosis, wound healing migration and transwell invasion assays. Then, an in vivo tumor formation assay was conducted to explore the effects of ADAMDEC1 on tumor growth.
Results
The mRNA and protein expression levels of ADAMDEC1 were upregulated in NSCLC tissues and cell lines. ADAMDEC1 expression was associated with clinicopathological characteristics and overall survival of patients with NSCLC. Knockdown of ADAMDEC1 could decrease proliferation and colony forming ability of NSCLC cells, and promoted cell apoptosis, whereas ADAMDEC11 overexpression has opposite effects in NSCLC cells both in vivo and in vitro. Furthermore, we identified ADAMDEC1 accelerates NSCLC progression via activation of the PI3K/ AKT pathway.
Conclusion
We verified that ADAMDEC1 promotes the progression of NSCLC via the PI3K/AKT pathway. These findings showed the potential of ADAMDEC1 to be used for therapeutic approaches in NSCLC.
Upregulated ADAMDEC1 in NSCLC is associated with poor prognosis. (a) Volcano plot chart showing the distribution of the DEGs in TCGA and GEO datasets. Upregulated genes are red; downregulated genes are green. (b) The expression level of ADAMDEC1 mRNA using RT‐PCR in NSCLC and normal tissues (n = 84); (c) The ADAMDEC1 protein expression level was significantly elevated in NSCLC tissues compared with adjacent normal tissues in selected 16 paired tissues. (d) ADAMDEC1 protein expression in NSCLC tissues and adjacent tissues (n = 16); (e) Representative images of ADAMDEC1 IHC staining of 84 patients in NSCLC and normal tissues (×400, scale bar 100 μm), respectively. (f) Overall survival curves for two groups defined by low and high expression of ADAMDEC1 in NSCLC patients. All results were representative of three separate experiments. ** p |
---|---|
ISSN: | 1759-7706 1759-7714 |
DOI: | 10.1111/1759-7714.14354 |