Evidence map›Paper›PMID 32567804›Full record

ArticleThoracic cancer2020

Identification of LBX2 as a novel causal gene of lung adenocarcinoma.

Jingwen Hu, Yongkang Bai, Quanli Zhang, Ming Li, Rong Yin, Lin Xu

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genetic Variants ofFrontiers in oncology · 2021
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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

6 authors at 1 institution in 1 country.

Jingwen HuDepartment of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Yongkang BaiDepartment of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Quanli ZhangDepartment of Scientific Research, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Ming LiDepartment of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Rong YinDepartment of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.
Lin XuDepartment of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, China.ORCID 0000-0002-2153-4840
Jiangsu Cancer Hospital · CN

Funding

Medical Foundation of the Affiliated Cancer Hospital of Nanjing Medical University ZN201606National Natural Science Foundation of China 81702265
6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is the most predominant histological type of lung cancer with a poor prognosis. In this study, we demonstrate that LBX2 regulates cell proliferation, migration and invasion and the potential molecular mechanism in LUAD.

methodsThe Cancer Genome Atlas dataset was accessed to screen for novel genes and immunohistochemistry (IHC) assays were performed to determine the association between LBX2 expression and clinicopathological features of LUAD. 5-ethynyl-2'-deoxyuridine, colony formation and Real Time xCELLigence analysis system were used to evaluate the cell proliferation abilities of LUAD. Wound healing, transwell and Matrigel assays were used to detect cell migration and invasion capacities. Xenograft tumor models were used to assess the oncogenic role of LBX2 in vivo.

resultsWe found that LBX2 was hyperexpressed in LUAD and correlated with clinicopathological features and poor prognosis in LUAD patients. Knockdown of LBX2 inhibited cell proliferation, migration and invasion of LUAD, whereas ectopic expression of LBX2 enhanced tumor growth, migration, and invasion. We further found that LBX2 might participate in epithelial-to-mesenchymal transition (EMT) progression and influence EMT-related gene expression.

conclusionsThe current study suggests that LBX2 plays an oncogenic role in LUAD and may participate in tumor proliferation, migration, and invasion through EMT progression. KEY POINTS: Significant findings of the study LBX2 might participate in LUAD cell proliferation, migration and invasion via EMT progression. What this study adds LBX2 may represent a potential biomarker and a promising therapeutic target for LUAD.

Indexed as

Adenocarcinoma of LungAnimalsFemaleHomeodomain ProteinsHumansLung NeoplasmsMaleMiceTransfectionHomeodomain ProteinsLBX2 protein, humanepithelial to mesenchymal transitionLBX2lung adenocarcinomaThe Cancer Genome Atlas

Identifiers

PMID32567804
PMCPMC7396393
OpenAlexW3036018155

What OpenQuestion holds

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LicenceCC BY
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.