Evidence map›Paper›PMID 34753517›Full record

ArticleBMC pharmacology & toxicology2021

Narciclasine induces autophagy-mediated apoptosis in gastric cancer cells through the Akt/mTOR signaling pathway.

Yunfeng Yuan, Xue He, Xiang Li, Yan Liu, Yueliang Tang, Huiming Deng, Xinyuan Shi

Open access · goldAbstract read
In one paragraph

Article in BMC pharmacology & toxicology, 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
1.4field-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. The multifaceted role of 3-methyladenine in cancer therapy.Journal of physiology and biochemistry · 2026
    Review
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  4. Frontiers in pharmacology · 2026
    Article
  5. Increasing autophagy activity suppressesAmerican journal of cancer research · 2026
    Article
  6. Article
  7. Article
  8. Article
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  10. Review
  11. Article
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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

7 authors at 3 institutions in 1 country.

Yunfeng Yuan *Department of Hepatobiliary Surgery, Chongqing Three Gorges Central Hospital, Chongqing University Three Gorges Hospital, No.165 Xincheng Road, Chongqing, 404000, China.
Xue He *Department of Hepatobiliary Surgery, Chongqing Three Gorges Central Hospital, Chongqing University Three Gorges Hospital, No.165 Xincheng Road, Chongqing, 404000, China.
Xiang LiDepartment of Hepatobiliary Surgery, Chongqing Three Gorges Central Hospital, Chongqing University Three Gorges Hospital, No.165 Xincheng Road, Chongqing, 404000, China.
Yan LiuDepartment of Hepatobiliary Surgery, Chongqing Three Gorges Central Hospital, Chongqing University Three Gorges Hospital, No.165 Xincheng Road, Chongqing, 404000, China.
Yueliang TangDepartment of General Surgery, Zengcheng District People's Hospital of Guangzhou, No.1 Guangming East Road, Guangzhou, 511300, China.
Huiming DengDepartment of General Surgery, Zengcheng District People's Hospital of Guangzhou, No.1 Guangming East Road, Guangzhou, 511300, China. dhm921008@163.com.
Xinyuan ShiDepartment of Gastroenterology, Taizhou First People's Hospital, No. 218 Hengjie Road, Taizhou, 318020, China. 18724213582@163.com.
Chongqing Three Gorges Central Hospital · CNChongqing University · CNTaizhou First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastric cancer is a common gastrointestinal cancer and currently has the third-highest mortality rate. Research shows that the natural compound narciclasine has a variety of biological activities. The present study aimed to investigate the effect of narciclasine on gastric cancer cells and its molecular mechanisms and determine whether this compound could be a novel therapy for gastric cancer.

methodsMTT and clone assays were employed to detect the proliferation of gastric cancer cells. The cell apoptosis was detected by flow cytometry. The formation of autophagosomes and autophagosomal lysosomes was observed by transmission electron microscopy and laser confocal scanning microscopy. Western blotting was used to detect the expression of apoptosis, autophagy and Akt/mTOR pathway-related proteins.

resultsIn this study, we found that narciclasine could inhibit the proliferation of gastric cancer cells and promote apoptosis in gastric cancer cells. Further experiments showed that narciclasine promoted the levels of autophagy proteins LC3-II, Atg-5 and Beclin-1, reduced the expression of the autophagy transporter p62, and increased autophagic flux. By using the autophagy inhibitors 3-MA and CQ, it was shown that narciclasine could induce autophagy-mediated apoptosis in gastric cancer cells. Finally, we found that narciclasine had no significant effects on the total content of Akt and mTOR in gastric cancer cells, and it involved autophagy in gastric cancer cells by reducing the phosphorylation level of p-Akt and p-mTOR.

conclusionsNarciclasine can induce autophagy-dependent apoptosis in gastric cancer cells by inhibiting the phosphorylation level of Akt/mTOR and thus reduce the proliferation of gastric cancer cells.

Indexed as

Amaryllidaceae AlkaloidsAntineoplastic Agents, PhytogenicApoptosisAutophagyCell Line, TumorCell ProliferationHumansPhenanthridinesProto-Oncogene Proteins c-aktSignal TransductionStomach NeoplasmsTOR Serine-Threonine KinasesAmaryllidaceae AlkaloidsAntineoplastic Agents, PhytogenicMTOR protein, humannarciclasinePhenanthridinesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAkt/mTOR pathwayApoptosisAutophagyGastric cancerNarciclasine

Identifiers

PMID34753517
PMCPMC8579652
OpenAlexW3213728328

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.