Evidence map›Paper›PMID 35968342›Full record

ArticleAmerican journal of cancer research2022

Interfering with ITGB1-DT expression delays cancer progression and promotes cell sensitivity of NSCLC to cisplatin by inhibiting the MAPK/ERK pathway.

Dan Li, Xiaoli Liu, Ni Jiang, Di Ke, Qiang Guo, Kui Zhai, Hao Han, Xue Xiao, Tengyang Fan

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.0field-weighted citation impact, top 12% 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, 2 syntheses or guidelines pooled it, 23 citations in OpenAlex.

  1. Pooled it
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    Review
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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

9 authors at 1 institution in 1 country.

Dan LiDepartment of General Medicine, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Xiaoli LiuDepartment of General Medicine, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Ni JiangCancer Laboratory, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Di KeDepartment of General Medicine, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Qiang GuoDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Kui ZhaiDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Hao HanDepartment of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Xue XiaoDepartment of General Medicine, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Tengyang FanDepartment of General Medicine, Affiliated Hospital of Zunyi Medical University Zunyi 563003, Guizhou, China.
Zunyi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA ITGB1-DT is involved in the regulation of cancer growth and metastasis. However, the roles of ITGB1-DT in non-small cell lung cancer (NSCLC) progression and sensitivity to cisplatin has not been elucidated. ITGB1-DT expression in NSCLC tissues, and the relationship between ITGB1-DT expression with NSCLC diagnosis, prognosis, clinicopathological features, and immune cell infiltration were investigated in The Cancer Gene Atlas (TCGA) database. The roles and mechanisms of ITGB1-DT in cell growth, migration, and drug sensitivity of NSCLC cells were explored in the cell model. The prognostic nomograms of ITGB1-DT-related genes were evaluated using bioinformatics. ITGB1-DT was overexpressed in NSCLC. Elevated ITGB1-DT expression was related to the late T stage, N stage, M stage, short overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI) of NSCLC patients. ITGB1-DT was the independent risk factors for poor prognosis, and had diagnostic value for NSCLC patients. Interfering with the ITGB1-DT expression can inhibit the proliferation, migration, and invasion of A549, H1299, and drug-resistant A549/DDP, possibly due to the inhibition of p38 MAPK and ERK phosphorylation levels. ITGB1-DT expression was correlated with the levels of NSCLC immune infiltration cells, such as the TReg, Th, and NK cells. ITGB1-DT-related gene nomograms were associated with the prognosis, and were expected to evaluate the prognosis of NSCLC patients. In conclusion, inhibition of ITGB1-DT expression delayed the growth and metastasis of NSCLC using the MAPK/ERK signaling mechanism and enhanced the sensitivity of NSCLC to cisplatin drugs. These results indicate that ITGB1-DT might be a biomarker for evaluating the diagnosis and prognosis of NSCLC patients.

Indexed as

disease-specific survivalITGB1-DTMAPKNSCLCoverall survivalprogression-free interval

Identifiers

PMID35968342
PMCPMC9360236
OpenAlexW4301385841

What OpenQuestion holds

Textmetadata
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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.