Evidence map›Paper›PMID 33362534›Full record

ArticleFrontiers in pharmacology2020

Quercetin Induces Apoptosis via Downregulation of Vascular Endothelial Growth Factor/Akt Signaling Pathway in Acute Myeloid Leukemia Cells.

Huan Shi, Xin-Yu Li, Yao Chen, Xing Zhang, Yong Wu, Zi-Xuan Wang, Pan-Hong Chen, Hui-Qi Dai, Ji Feng, Sayantan Chatterjee and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 53 citations in OpenAlex.

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  12. Phenolic Compounds inMolecules (Basel, Switzerland) · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Huan ShiDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Xin-Yu LiDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Yao ChenDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Xing ZhangArtemisinin Research Center and the Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.
Yong WuDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, China.
Zi-Xuan WangDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, China.
Pan-Hong ChenDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Hui-Qi DaiDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, China.
Ji FengDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, China.
Sayantan ChatterjeeDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Zhong-Jie LiDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Xiao-Wei HuangDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, China.
Hong-Qiao WeiDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Jigang WangArtemisinin Research Center and the Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing, China.
Guo-Dong LuDepartment of Toxicology, School of Public Health, Guangxi Medical University, Nanning, China.
Jing ZhouDepartment of Physiology, School of Preclinical Medicine, Guangxi Medical University, Nanning, China.
Guangxi Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNHunan University · CNTumor Hospital of Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukemia (AML) is an aggressive haematological malignancy characterized by highly proliferative accumulation of immature and dysfunctional myeloid cells. Quercetin (Qu), one kind of flavonoid, exhibits anti-cancer property in multiple types of solid tumor, but its effect on acute myeloid leukemia is less studied, and the underlying mechanisms still largely unknown. This study aimed to explore the specific target and potential mechanism of quercetin-induced cell death in AML. First, we found that quercetin induces cell death in the form of apoptosis, which was caspase dependent. Second, we found that quercetin-induced apoptosis depends on the decrease of mitochondria membrane potential (MMP) and Bcl-2 proteins. With quantitative chemical proteomics, we observed the downregulation of VEGFR2 and PI3K/Akt signaling in quercetin-treated cells. Consistently, cell studies also identified that VEGFR2 and PI3K/Akt signaling pathways are involved in the action of quercetin on mitochondria and Bcl-2 proteins. The decrease of MMP and cell death could be rescued when PI3K/Akt signaling is activated, suggesting that VEGFR2 and PI3K/Akt exert as upstream regulators for quercetin effect on apoptosis induction in AML cells. In conclusion, our findings from this study provide convincing evidence that quercetin induces cell death via downregulation of VEGF/Akt signaling pathways and mitochondria-mediated apoptosis in AML cells.

Indexed as

acute myeloid leukemiaapoptosismitochondriaquercetinvascular endothelial growth factor/PI3K/Akt

Identifiers

PMID33362534
PMCPMC7758733
OpenAlexW3112422024

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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.