Evidence map›Paper›PMID 32104250›Full record

ArticleExperimental and therapeutic medicine2020

Knockdown of TOR signaling pathway regulator suppresses cell migration and invasion in non-small cell lung cancer via the regulation of epithelial-to-mesenchymal transition.

Xiang Xu, Huangkai Zhu, Minglei Yang, Enkuo Zheng, Yinjie Zhou, Junjun Ni, Rui Li, Zhenhua Yang, Ti He, Guofang Zhao

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Review
  7. Journal of thoracic disease · 2023
    Article
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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

10 authors at 1 institution in 1 country.

Xiang XuDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Huangkai ZhuDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Minglei YangDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Enkuo ZhengDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Yinjie ZhouDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Junjun NiDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Rui LiDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Zhenhua YangDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
Ti HeShanghai Genechem Translational Medicine Institute, Shanghai 200120, P.R. China.
Guofang ZhaoDepartment of Cardiothoracic Surgery, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo, Zhejiang 315010, P.R. China.
University of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is one of the most common cancer types worldwide. Previous studies have indicated that TOR signaling pathway regulator (TIPRL) is involved in the progression of NSCLC. However, the underlying mechanisms of the role of TIPRL in regulating NSCLC metastasis have remained largely elusive. In the present study, the expression pattern of TIPRL in NSCLC was analyzed using The Cancer Genome Atlas (TCGA) dataset. Furthermore, Kaplan-Meier curve analysis was performed to evaluate the prognostic value of TIPRL in NSCLC, using the Kaplan-Meier Plotter and TCGA datasets. Loss-of-function assays were performed to determine the effects of TIPRL on cell migration and invasion. The results suggested that TIPRL was upregulated in NSCLC and positively associated with an advanced Tumor-Node-Metastasis stage. A higher expression level of TIPRL was associated with shorter overall and disease-free survival times in patients with NSCLC. To the best of our knowledge, the present study was the first to report that TIPRL acts as a metastasis promoter in NSCLC. Silencing of TIPRL suppressed A549 cell migration and invasion. Mechanistically, the present study indicated that TIPRL knockdown significantly promoted epithelial-cadherin expression, whereas it suppressed twist and vimentin expression in A549 cells. In conclusion, the present analysis suggested that TIPRL may serve as a biomarker for the prognosis of NSCLC and as a future target for its treatment.

Indexed as

epithelial-to-mesenchymal transitioninvasionmigrationnon-small cell lung cancerTOR signaling pathway regulator

Identifiers

PMID32104250
PMCPMC7027157
OpenAlexW2995427375

What OpenQuestion holds

Textmetadata
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.