Evidence map›Paper›PMID 36157221›Full record

ArticleDisease markers2022

EIF3C Promotes Lung Cancer Tumorigenesis by Regulating the APP/HSPA1A/LMNB1 Axis.

Xiaoli Ding, Lanlan Hou, Huijuan Zhang, Zhiping Chen, Zhanyu Liu, Junjie Gong, Zhixian Tang, Rong Hu

Open access · hybridAbstract read
In one paragraph

Article in Disease markers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
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 2 institutions in 1 country.

Xiaoli DingDepartment of Clinical Examination, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.
Lanlan HouGannan Medical University, Ganzhou, Jiangxi 341000, China.
Huijuan ZhangDepartment of Clinical Examination, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.
Zhiping ChenDepartment of Clinical Examination, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.
Zhanyu LiuDepartment of Clinical Examination, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.
Junjie GongDepartment of Clinical Examination, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.
Zhixian TangThoracic Surgery, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.ORCID https://orcid.org/0000-0001-6250-7139
Rong HuDepartment of Clinical Examination, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, China.ORCID https://orcid.org/0000-0002-6188-9312
First Affiliated Hospital of Gannan Medical University · CNGannan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: This study was designed to explore the role and mechanism of eukaryotic initiation factor 3C (EIF3C) in the proliferation and apoptosis of lung cancer cells. Methods: EIF3C expression in clinic lung cancer tissues was detected by immunohistochemistry assay. Cell transfection with lentivirus EIF3C short hairpin RNA (shRNA) was performed with Lipofectamine 2000. Cell proliferation was evaluated by Celigo and MTT assays. Caspase-3/7 activity was assessed using caspase-3/7 assay kit for cell apoptosis detection. The apoptosis rate of lung cancer cells was assessed by flow cytometry. A transplanted tumor nude-mouse model was established to clarify the role of EIF3C in lung cancer. The potential mechanism of EIF3C was explored by mRNA microarray analysis. Among the top 30 up- and downregulated mRNAs selected for RT-qPCR, 5 were chosen for western blot analysis. Results: EIF3C was abnormally overexpressed in lung cancer cell lines and tissues. Silencing EIF3C suppressed the proliferation and promoted the apoptosis of lung cancer cells. Conclusion: EIF3C overexpression may facilitate the proliferation and hamper the apoptosis of lung cancer cells by regulating the APP/HSPA1A/LMNB1 axis.

Indexed as

Eukaryotic Initiation Factor-3Lung NeoplasmsAnimalsApoptosisCarcinogenesisCaspase 3Cell Line, TumorCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticMiceMice, NudeRNA, MessengerRNA, Small InterferingCaspase 3Eukaryotic Initiation Factor-3RNA, MessengerRNA, Small Interfering

Identifiers

PMID36157221
PMCPMC9492341
OpenAlexW4295957079

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.