Evidence map›Paper›PMID 37277814›Full record

ArticleBiology direct2023

ANKRD29, as a new prognostic and immunological biomarker of non-small cell lung cancer, inhibits cell growth and migration by regulating MAPK signaling pathway.

Hanqing Zhao, Yanbo Wang, Yaomei He, Peng Zhang, Cheng Zeng, Tongxuan Du, Qiushuo Shen, Song Zhao

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

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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

7 citing papers in PubMed, 7 citations in OpenAlex.

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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

8 authors at 4 institutions in 1 country.

Hanqing Zhao *Department of Thoracic Surgery, the First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Yanbo Wang *Department of Thoracic Surgery, the First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Yaomei He *Yan'an Hospital Affiliated to Kunming Medical University, Kunming, China.
Peng ZhangDepartment of Thoracic Surgery, the First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Cheng ZengDepartment of Thoracic Surgery, the First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China.
Tongxuan DuInstitute of Biomedical Engineering, Kunming Medical University, 650500, Kunming, Yunnan, China.
Qiushuo ShenDepartment of Thoracic Surgery, the First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China. shenqiushuo@126.com.
Song ZhaoDepartment of Thoracic Surgery, the First Affiliated Hospital of Zhengzhou University, 450052, Zhengzhou, China. zhaosong@zzu.edu.cn.
First Affiliated Hospital of Zhengzhou University · CNKunming Medical University · CNYan'an Hospital Affiliated To Kunming Medical University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe predominant cancer-related deaths worldwide are caused by lung cancer, particularly non-small cell lung cancer (NSCLC), despite the fact that numerous therapeutic initiatives have been devised to improve the outcomes. Ankyrin repeat domain (ANKRD) is one of the widespread protein structural motifs in eukaryotes but the functions of ANKRD proteins in NSCLC progression remains unclear.

methodsWe performed integrative bioinformatical analysis to determine the dysregulated expression of ANKRDs in multiple tumors and the association between ANKRD29 expression and the NSCLC tumor environment. Quantitative real-time PCR (qRT-PCR), western blot, immunohistochemistry (IHC), and tissue microarray (TMA) assays were used to investigate the expression of ANKRD29 in NSCLC cell lines. The role of ANKRD29 in NSCLC cell proliferation and migration in vitro was deteceted by 5-bromodeoxyuridine (BrdU) incorporation, colony formation, flow cytometry, would-healing, trans-well, and western blot experiment. RNA-seq technology was applied to deciper the molecular mechanism regulated by ANKRD29 in NSCLC.

resultsWe constructed a valuable risk-score system for predicting the overall survival outcomes of NSCLC patients based on the expression of five hub ANKRD genes. And we found that the hub gene ANKRD29 was remarkedly decreased in NSCLC tissues and cell lines due to the promoter hypermethylation, and revealed that high ANKRD29 expression obviously correlated with patients' better clinical outcome. Overexpression of ANKRD29 significantly inhibited cell proliferation and migration, promoted the cancerous cells' sensitivity to carboplatin and enhanced the killing ability of T cells in NSCLC cells. Interestingly, ANKRD29 can be served as a biomarker to predict the response to immunotherapy in NSCLC. Mechanically, RNA-seq results showed that ANKRD29 could regulate MAPK signaling pathway. Moreover, we screened two potential agonists for ANKRD29.

conclusionsANKRD29 functions as a new tumor suppressor in NSCLC tumorigenesis and could be developed as a biomarker for prognostic prediction, immunotherapy response, and drug susceptibility evaluation of NSCLC in the future.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsBiomarkersCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsPrognosisSignal TransductionANKRD29 protein, humanBiomarkersIntracellular Signaling Peptides and ProteinsANKRD29BiomarkerCell growth and migrationImmune therapy responseNon–small cell lung cancer

Identifiers

PMID37277814
PMCPMC10243072
OpenAlexW4379509116

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Registered trials

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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.