Evidence map›Paper›PMID 32130676›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2020

PRDX2 plays an oncogenic role in esophageal squamous cell carcinoma via Wnt/β-catenin and AKT pathways.

A L Feng, X Han, X Meng, Z Chen, Q Li, W Shu, H Dai, J Zhu, Z Yang

Abstract read
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In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

17 citing papers in PubMed, 53 citations in OpenAlex.

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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 3 institutions in 1 country.

A L FengDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China.
X HanExperimental Department, Affiliated Tumor Hospital of Guangxi Medical University, 71# Hedi Road, Nanning, 530021, People's Republic of China.
X MengDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China.
Z ChenDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China.
Q LiDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China.
W ShuDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China.
H DaiDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China.
J ZhuDepartment of General Surgery, The First Affiliated Hospital of Shandong First Medical University, 16766# Jingshi Road, Jinan, 250014, People's Republic of China. 249217523@qq.com.
Z YangDepartment of Oncology, Shandong Provincial Hospital Affiliated To Shandong University, 324# Jing 5 Road, Jinan, 250021, People's Republic of China. yangzsl@126.com.ORCID http://orcid.org/0000-0002-2649-3208
Shandong University · CNJining First People's Hospital · CNTumor Hospital of Guangxi Medical University · CN

Funding

National Natural Science Foundation of China 81500496National Natural Science Foundation of China 81502508
6 · The paper itself

Abstract

purposeTo investigate the role of PRDX2 in esophageal carcinoma (ESCA).

methodsThe expression of PRDX2 was detected in ESCA tissues. And PRDX2 expression in two ESCA cell lines was knocked down. Cell proliferation, metastasis and invasion were detected in these cells.

resultsHere, we found that PRDX2 expression was significantly increased in ESCA tissues and was associated with a poor prognosis in ESCA patients. In addition, PRDX2 expression was significantly associated with pathological grading, infiltration degree and 5-year survival time in ESCA patients. Next, we knocked down PRDX2 expression by PRDX2-shRNA transfection in two ESCA cell lines, Eca-109 and TE-1. Proliferation analysis indicated that in vitro PRDX2 knockdown decreased growth and clone formation of ESCA cells. Scratch and transwell assays indicated that cell migration and invasion were significantly inhibited by PRDX2 knockdown. In addition, PRDX2 knockdown inhibited cell cycle of ESCA cells and down-regulated Cyclin D1-CDK4/6. Moreover, PRDX2 knockdown regulated proteins involved in mitochondrial-dependent apoptosis, including increased Bax and Caspase9/3 and decreased Bcl2. Mechanism investigation indicated that PRDX2 knockdown led to inactivation of Wnt/β-catenin and AKT pathways.

conclusionsOur data suggest that PRDX2 may function as an oncogene in the development of ESCA via regulating Wnt/β-catenin and AKT pathways. Our study fills a gap in the understanding of the role of PRDX2 in ESCA and provides a potential target for ESCA treatment.

Indexed as

ApoptosisCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansPeroxiredoxinsProto-Oncogene Proteins c-aktWnt Signaling PathwayPeroxiredoxinsPRDX2 protein, humanProto-Oncogene Proteins c-aktApoptosisEsophageal carcinomaPeroxiredoxin 2Protein kinase BWnt/β-catenin

Identifiers

PMID32130676
OpenAlexW3009844968

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.