Evidence map›Paper›PMID 32477104›Full record

ArticleFrontiers in pharmacology2020

A Novel Benzofuran Derivative Moracin N Induces Autophagy and Apoptosis Through ROS Generation in Lung Cancer.

Chengcheng Gao, Xin Sun, Zhipan Wu, Huahua Yuan, Haote Han, Hongliang Huang, Yuhan Shu, Mengting Xu, Ruilan Gao, Shouxin Li and 2 more

Open 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. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-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

21 citing papers in PubMed, 40 citations in OpenAlex.

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  12. Pennogenin-3-Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  13. ACS omega · 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

12 authors at 5 institutions in 2 countries.

Chengcheng GaoCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Xin SunClinical Research Institute, Key Laboratory of Tumor Molecular Diagnosis and Individual Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Zhipan WuCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Huahua YuanCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Haote HanCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Hongliang HuangSchool of Biosciences & Biopharmaceutics and Center for Bioresources & Drug Discovery, Guangdong Pharmaceutical University, Guangzhou, China.
Yuhan ShuCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Mengting XuCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Ruilan GaoInstitution of Hematology Research, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
Shouxin LiCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Jianbin ZhangClinical Research Institute, Key Laboratory of Tumor Molecular Diagnosis and Individual Medicine of Zhejiang Province, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Jingkui TianCollege of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Zhejiang University · CNHangzhou Medical College · CNGuangdong Pharmaceutical University · CNZhejiang Chinese Medical University · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe leaves of

objectiveIn this study, we aimed to examine the effect of MAN on human lung cancer and reveal the underlying molecular mechanism.

methodsMTT assay was conducted to measure cell viability. Annexin V-FITC/PI staining was used to detect cell apoptosis. Confocal microscope was performed to determine the formation of autophagosomes and autolysosomes. Flow cytometry was performed to quantify cell death. Western blotting was used to determine the related-signaling pathway.

resultsIn the present study, we demonstrated for the first time that MAN inhibitd cell proliferation and induced cell apoptosis in human non-small-cell lung carcinoma (NSCLC) cells. We found that MAN treatment dysregulated mitochondrial function and led to mitochondrial apoptosis in A549 and PC9 cells. Meanwhile, MAN enhanced autophagy flux by the increase of autophagosome formation, the fusion of autophagsomes and lysosomes and lysosomal function. Moreover, mTOR signaling pathway, a classical pathway regualting autophagy, was inhibited by MAN in a time- and dose-dependent mannner, resulting in autophagy induction. Interestingly, autophagy inhibition by CQ or Atg5 knockdown attenuated cell apoptosis by MAN, indicating that autophagy serves as cell death. Furthermore, autophagy-mediated cell death by MAN can be blocked by reactive oxygen species (ROS) scavenger NAC, indicating that ROS accumulation is the inducing factor of apoptosis and autophagy. In summary, we revealed the molecular mechanism of MAN against lung cancer through apoptosis and autophagy, suggesting that MAN might be a novel therapeutic agent for NSCLC treatment.

Indexed as

autophagymitochondrial apoptosisMoracin NmTORreactive oxygen species

Identifiers

PMID32477104
PMCPMC7235196
OpenAlexW3025395387

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.