Evidence map›Paper›PMID 33819194›Full record

ArticleAging2021

The critical role of peroxiredoxin-2 in colon cancer stem cells.

Linglong Peng, Yongfu Xiong, Rong Wang, Ling Xiang, He Zhou, Zhongxue Fu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. PRX5 as a critical driver of colorectal cancer stemness and tumorigenicity.Redox report : communications in free radical research · 2026
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  13. The beginning of GPX2 and 30 years later.Free radical biology & medicine · 2022
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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

6 authors at 5 institutions in 1 country.

Linglong PengDepartment of Gastrointestinal Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China.
Yongfu XiongDepartment of Hepatobiliary Surgery, The Affiliated Hospital of North Sichuan Medical College, Sichuan 637000, China.
Rong WangDepartment of Oncology, The Cancer Center of the Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China.
Ling XiangDepartment of Clinical Nutrition, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China.
He ZhouDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China.
Zhongxue FuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400014, China.
Chongqing Medical University · CNAffiliated Hospital of North Sichuan Medical College · CNFirst Affiliated Hospital of Chongqing Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colon cancer stem cells (CCSCs) play an important role in facilitating colon cancer occurrence, metastasis and drug resistance. The results of our previous studies confirmed that the well-studied antioxidant gene peroxiredoxin-2 (PRDX2) promotes colon cancer progression. However, the underlying function and mechanisms associated with PRDX2 remodeling in the context of CCSCs have remained poorly studied. In our present study, we demonstrated that PRDX2 is highly expressed in CD133/CD44-positive colon cancer tissues and spheroid CD133+CD44+ CCSCs. PRDX2 overexpression was shown to be closely correlated with CD133+CD44+ CCSCs in colon cancer. Furthermore, PRDX2 depletion markedly suppressed CD133+CD44+ CCSC stemness maintenance, tumor initiation, migration and invasion and liver metastasis. Furthermore, the expression of various EMT markers and Wnt/β-catenin signaling proteins was altered after PRDX2 inhibition. In addition, PRDX2 knockdown led to increased ROS production in CD133+CD44+ CCSCs, sensitizing CCSCs to oxidative stress and chemotherapy. These results suggest that PRDX2 could be a possible therapeutic target in CCSCs.

Indexed as

AnimalsColonColonic NeoplasmsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHCT116 CellsHT29 CellsHumansLiver NeoplasmsMiceNeoplastic Stem CellsPeroxiredoxinsSpheroids, CellularXenograft Model Antitumor AssaysPeroxiredoxinsPRDX2 protein, humanchemoresistancecolon cancercolon cancer stem cellsmetastasisperoxiredoxin-2

Identifiers

PMID33819194
PMCPMC8109100
OpenAlexW3143260701

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.