Evidence map›Paper›PMID 36317123›Full record

ArticleJournal of oncology2022

IMP4 Silencing Inhibits the Malignancy of Lung Adenocarcinoma via ERK Pathway.

Ruzhen Li, Zhaohui Han, Wei Ma, Lin Zhang, Xiangwei Zhang, Yuanzhu Jiang, Wei Dong

Open access · hybridAbstract read
In one paragraph

Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
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 1 institution in 1 country.

Ruzhen LiDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0002-8973-6617
Zhaohui HanDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0001-6727-9307
Wei MaDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0003-0404-4687
Lin ZhangDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0002-6724-6529
Xiangwei ZhangDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0001-6459-2752
Yuanzhu JiangDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0003-2007-4050
Wei DongDepartment of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.ORCID https://orcid.org/0000-0002-8107-3900
Shandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our study aimed to elucidate the function of IMP U3 small nucleolar ribonucleoprotein 4 (IMP4) in lung adenocarcinoma (LUAD) and its potential molecular mechanisms. Cell counting kit-8, 5-ethynyl-20-deoxyuridine, flow cytometry, wound healing, and transwell assays were performed to examine the biological behaviour of LUAD cells. mRNA and protein expression levels were determined using quantitative real-time PCR, Western blotting, and immunohistochemistry. In addition, a mouse tumour xenograft model was used to evaluate the role of IMP4 in tumour progression. Furthermore, glycolysis-related indicators were measured. The levels of IMP4 were up-regulated in both human LUAD tissues and cells. IMP4 silencing significantly suppressed proliferation, migration, invasion, and glycolysis; promoted apoptosis; and induced cell cycle arrest in LUAD cells. IMP4 silencing also inactivated the extracellular signal-regulated kinase (ERK) pathway. Moreover, rescue experiments demonstrated that the function of LUAD cells induced by IMP4 overexpression could be reversed by treatment with an ERK pathway inhibitor (SCH772984).

Identifiers

PMID36317123
PMCPMC9617734
OpenAlexW4307136583

What OpenQuestion holds

Textmetadata
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.