Evidence map›Paper›PMID 30106131›Full record

ArticleInternational journal of molecular medicine2018

Upregulation of HOXA11 during the progression of lung adenocarcinoma detected via multiple approaches.

Xia Yang, Yun Deng, Rong-Quan He, Xiao-Jiao Li, Jie Ma, Gang Chen, Xiao-Hua Hu

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

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  13. Expression Profile and Prognostic Values ofFrontiers in oncology · 2020
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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

7 authors at 2 institutions in 1 country.

Xia YangDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Yun DengDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Rong-Quan HeDepartment of Medical Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Xiao-Jiao LiDepartment of Positron Emission Tomography‑Computed Tomography, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Jie MaDepartment of Medical Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Gang ChenDepartment of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Xiao-Hua HuDepartment of Medical Oncology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The altered expression of homeobox (HOX)A11 has been observed in various malignant tumor types, but it has remained to be determined in human lung adenocarcinoma (LUAD). In the present study, the expression of HOXA11 in LUAD and the potential associated mechanisms were assessed. Data from The Cancer Genome Atlas and Oncomine microarrays were gathered and in‑house polymerase chain reaction data were produced to investigate the altered expression of HOXA11 in LUAD and its association with various clinicopathological characteristics. Genes co‑expressed with HOXA11 were also identified by searching the cBioPortal and Multi Experiment Matrix databases, and performing a bioinformatics analysis, through which the potential molecular mechanisms of HOXA11 in LUAD were explored. The data analyses indicated that HOXA11 was overexpressed in the LUAD samples, and together with its co‑expressed genes, it was indicated to participate in various key signaling pathways, including the focal adhesion, extracellular matrix‑receptor interaction, axon guidance and small cell lung cancer signaling pathways. Furthermore, collagen type III α 1 chain (COL3A1), ephrin B2 (EFNB2), integrin subunit α 8 (ITGA8) and syndecan 2 (SDC2) were confirmed to be differentially expressed in LUAD vs. normal controls at the mRNA and protein level. Of note, LUAD patients with low expression of HOXA11 and ITGB1 had better overall survival rates. The present study indicated that HOXA11 may function as an oncogene in LUAD, and HOXA11 protein probably combines with ITGB1, COL3A1, EFNB2, ITGA8 and SDC2 to have a role in the focal adhesion pathway.

Indexed as

Adenocarcinoma of LungAdultAgedAged, 80 and overCollagen Type IIIComputational BiologyEphrin-B2Homeodomain ProteinsHumansIntegrin alpha ChainsLung NeoplasmsMiddle AgedSyndecan-2COL3A1 protein, humanCollagen Type IIIEFNB2 protein, humanEphrin-B2Homeodomain ProteinsHOXA11 protein, humanIntegrin alpha ChainsITGA8 protein, humanSDC2 protein, humanSyndecan-2

Identifiers

PMID30106131
PMCPMC6192730
OpenAlexW2887539836

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.