Evidence map›Paper›PMID 35388733›Full record

ArticleInternational journal of immunopathology and pharmacology

Evodiamine suppresses the progression of non-small cell lung carcinoma via endoplasmic reticulum stress-mediated apoptosis pathway

Yuting Li, Yuming Wang, Xiaoqun Wang, Lulu Jin, Lu Yang, Jinli Zhu, Hongwu Wang, Fang Zheng, Huantian Cui, Xiaojiang Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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  3. Comprehensive Analysis of 11 Species ofMolecules (Basel, Switzerland) · 2024
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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

11 authors at 3 institutions in 1 country.

Yuting LiFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Yuming WangFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Xiaoqun Wang74770National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, China.
Lulu JinFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Lu YangFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Jinli Zhu74770National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, China.
Hongwu WangFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Fang ZhengFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Huantian CuiShandong Provincial Key Laboratory of Animal Cell and Developmental Biology, School of Life Sciences, 12589Shandong University, Qingdao, China.ORCID https://orcid.org/0000-0002-0820-5436
Xiaojiang Li74770National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, China.
Yingjie Jia74770National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, China.
First Teaching Hospital of Tianjin University of Traditional Chinese Medicine · CNTianjin University of Traditional Chinese Medicine · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEvodiamine (EVO) is one of the major components isolated from

objectivesThis study focused on asking the anti-cancer effect of EVO in human non-small cell lung carcinoma (NSCLC), and in particular to investigate whether EVO acts via modulating the endoplasmic reticulum stress (ERS)-mediated apoptosis pathway. MATERIALS AND

methodsA Lewis lung carcinoma (LLC) tumor-bearing mouse model was treated with low-dose EVO (5 mg/kg) and high-dose EVO (10 mg/kg) intraperitoneally for 14 d. The effects of EVO on tumor growth, apoptosis, and ERS were assessed. In addition, NSCLC A549 and LLC cells were treated with EVO in vitro. The effects of EVO on cell proliferation, apoptosis, and ERS were investigated. Finally, 4-phenylbutyric acid (4-PBA), an ERS inhibitor, was used to validate whether EVO induced apoptosis of NSCLC cells by modulating ERS.

resultsEVO treatment significantly inhibited tumor growth in LLC tumor-bearing mice. H&E staining indicated that EVO treatment reduced the number of tumor cells and the nucleo-plasmic ratio. Immunostaining showed that EVO treatment significantly decreased the expression of Ki-67. TUNEL staining revealed that EVO induced apoptosis in the tumor. Likewise, EVO treatment up-regulated the expression of apoptosis-related genes and proteins and increased activation of the ERS pathway in the tumor. Additionally, EVO inhibited cell proliferation and increased cell apoptotic rates in A549 and LLC cells. EVO also increased the expression levels of genes and proteins associated with ERS-mediated apoptosis pathway in vitro. The effects of EVO on apoptosis were abolished by 4-PBA treatment.

conclusionsOur study demonstrated that EVO suppresses the progression of NSCLC by modulating the ERS-mediated apoptosis pathway.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAnimalsApoptosisCell Line, TumorEndoplasmic Reticulum StressMiceQuinazolinesevodiamineQuinazolinesA549 cellsapoptosisendoplasmic reticulum stressEvodiaminelewis lung carcinoma cellsnon-small cell lung carcinoma

Identifiers

PMID35388733
PMCPMC9003648
OpenAlexW4223417381

What OpenQuestion holds

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Registered trials

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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.