Evidence map›Paper›PMID 33006362›Full record

ArticleBioscience reports2020

Knockdown of CRAD suppresses the growth and promotes the apoptosis of human lung cancer cells via Claudin 4.

Anfang Cui, Yuchan Xue, Xi'ao Wang, Yanhong Huang, Xiaolin Han, Xiangling Li, Delei Niu, Shaorui Niu, Yujie Zhao, Xinyu Yang and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Claudin-4: A New Molecular Target for Epithelial Cancer Therapy.International journal of molecular sciences · 2023
    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

11 authors at 1 institution in 1 country.

Anfang CuiCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Yuchan XueCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Xi'ao WangCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Yanhong HuangCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Xiaolin HanCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Xiangling LiCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Delei NiuInstitute of Forensic Medicine and Laboratory Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Shaorui NiuCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Yujie ZhaoInstitute of Forensic Medicine and Laboratory Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Xinyu YangCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Wei YuCollege of Basic Medicine, Jining Medical University, Jining, Shandong 272067, P.R. China.
Jining Medical University · 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 causes of cancer-related mortality globally. However, the mechanism underlying NSCLC is not fully understood. Here, we investigated the role of cancer-related regulator of actin dynamics (CRAD) in NSCLC. We showed that CRAD was up-regulated in human NSCLC tissues and lung cancer cell lines. Lentivirus-mediated knockdown of CRAD repressed the proliferation and colony growth of A549 and H1299 cells. Apoptosis was enhanced by CRAD silencing in both cells, implicating that CRAD might maintain the survival of lung cancer cells. Microarray and bioinformatic assay revealed that CRAD directly or indirectly regulated diverse genes, including those involved in cell cycle and DNA damage repair. qRT-PCR and Western blot results confirmed the dysregulated genes as shown in microarray analysis. Claudin 4 was up-regulated in CRAD silenced A549 cells. The knockdown of Claudin 4 blocked the effects of CRAD on the expression of cell cycle and apoptosis effectors and enhanced the viability of A549 cells with CRAD down-regulation. Taken together, our findings demonstrate that CRAD acts as an oncogene in NSCLC at least partly through repressing Claudin 4.

Indexed as

A549 CellsApoptosisCarcinoma, Non-Small-Cell LungCell CycleCell ProliferationClaudin-4Computational BiologyDNA DamageDNA RepairGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLungLung NeoplasmsMicrofilament ProteinsClaudin-4CLDN4 protein, humanCRACD protein, humanMicrofilament ProteinsApoptosisCARDClaudin 4NSCLCProliferation

Identifiers

PMID33006362
PMCPMC7560521
OpenAlexW3089879462

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.