Evidence map›Paper›PMID 35178875›Full record

ArticleThoracic cancer2022

Upregulation of ADAMDEC1 correlates with tumor progression and predicts poor prognosis in non-small cell lung cancer (NSCLC) via the PI3K/AKT pathway.

Weiliang Zhu, Lin Shi, Yuxin Gong, Lin Zhuo, Siyun Wang, Shaobing Chen, Bei Zhang, Bin Ke

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. International journal of general medicine · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. ADAMDEC1 accelerates GBM progressionFrontiers in oncology · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Weiliang ZhuDepartment of Cancer Center, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Lin ShiDepartment of Traditional Chinese Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Yuxin GongDepartment of Traditional Chinese Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Lin ZhuoDepartment of Traditional Chinese Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Siyun WangDepartment of Traditional Chinese Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Shaobing ChenDepartment of Traditional Chinese Medicine, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong, China.
Bei ZhangDepartment of VIP Region, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.
Bin KeDepartment of VIP Region, State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, China.ORCID 0000-0001-6242-9898
Zhujiang Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundADAM-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.

methodsWe 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.

resultsThe 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.

conclusionWe 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.

Indexed as

ADAM ProteinsCarcinoma, Non-Small-Cell LungLung NeoplasmsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene Proteins c-aktSignal TransductionUp-RegulationADAM ProteinsdecysinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktADAMDEC1apoptosisnon-small cell lung cancerprognosisproliferation

Identifiers

PMID35178875
PMCPMC8977174
OpenAlexW4213213236

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.