Evidence map›Paper›PMID 35840666›Full record

ArticleCancer gene therapy2022

Nrf2 overexpression increases the resistance of acute myeloid leukemia to cytarabine by inhibiting replication factor C4.

Tianzhen Hu, Chengyun Pan, Tianzhuo Zhang, Ming Ni, Weili Wang, Siyu Zhang, Ying Chen, Jishi Wang, Qin Fang

RetractedErratum issuedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Tianzhen HuCollege of Pharmacy, Guizhou Medical University, Guiyang, Guizhou, China.
Chengyun PanDepartment of Haematology, Affiliated Hospital of Guizhou Medical University, Guizhou Province Institute of Hematology, Guiyang, Guizhou, China.
Tianzhuo ZhangSchool of Basic Medical Sciences, Guizhou Medical University, Guiyang, Guizhou, China.
Ming NiDepartment of Haematology, Affiliated Hospital of Guizhou Medical University, Guizhou Province Institute of Hematology, Guiyang, Guizhou, China.
Weili WangDepartment of Haematology, Affiliated Hospital of Guizhou Medical University, Guizhou Province Institute of Hematology, Guiyang, Guizhou, China.ORCID http://orcid.org/0000-0002-8642-3447
Siyu ZhangCollege of Pharmacy, Guizhou Medical University, Guiyang, Guizhou, China.
Ying ChenDepartment of Haematology, Affiliated Hospital of Guizhou Medical University, Guizhou Province Institute of Hematology, Guiyang, Guizhou, China.
Jishi WangDepartment of Haematology, Affiliated Hospital of Guizhou Medical University, Guizhou Province Institute of Hematology, Guiyang, Guizhou, China. wangjishi9646@163.com.ORCID http://orcid.org/0000-0001-5118-6990
Qin Fangpharmacy department, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China. fangqin@gmc.edu.cn.ORCID http://orcid.org/0000-0001-9492-5204
Guiyang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance is a key factor in the treatment failure of acute myeloid leukemia (AML). Nuclear factor E2-related factor 2 (Nrf2) plays a crucial role in tumor chemotherapy resistance. However, the potential mechanism of Nrf2 regulating DNA mismatch repair (MMR) pathway to mediate gene-instability drug resistance in AML is still unclear. Here, it was found that Nrf2 expression was closely related to the disease progression of AML as well as highly expressed in AML patients with poor prognostic gene mutations. Meanwhile, it was also found that the expression of Nrf2 was significantly negatively correlated with DNA MMR gene replication factor C4 (RFC4) in AML. CHIP analysis combined with luciferase reporter gene results further showed that Nrf2 may inhibit the expression of RFC4 by its interaction with the RFC4 promoter. In vitro and vivo experiments showed that the overexpression of Nrf2 decreased the killing effect of chemotherapy drug cytarabine (Ara-C) on leukemia cells and inhibited the expression of RFC4. Mechanistically, The result that Nrf2-RFC4 axis mediated AML genetic instability drug resistance might be received by activating the JNK/NF-κB signaling pathway. Taken together, these findings may provide a new idea for improving AML drug resistance.

Indexed as

CytarabineLeukemia, Myeloid, AcuteCell Line, TumorDrug Resistance, NeoplasmHumansNF-E2-Related Factor 2NF-kappa BCytarabineNF-E2-Related Factor 2NF-kappa B

Identifiers

PMID35840666
PMCPMC9663296
OpenAlexW4285492259

What OpenQuestion holds

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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.