Evidence map›Paper›PMID 28450693›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Lycorine Induces Apoptosis of A549 Cells via AMPK-Mammalian Target of Rapamycin (mTOR)-S6K Signaling Pathway.

Hui Zeng, Rong Fu, Linxia Yan, Jian Huang

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.5field-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

9 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Structure, function, and pathology of PHF23.Frontiers in cell and developmental biology · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Lycorine: A prospective natural lead for anticancer drug discovery.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2018
    Review
  9. Article
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

4 authors at 2 institutions in 1 country.

Hui ZengDepartment of Medicine, Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan, China (mainland).
Rong FuDepartment of Plastic Surgery, Sichuan Provincial People's Hospital, Chengdu, Sichuan, China (mainland).
Linxia YanChengdu Lilai Biotechnology Co., Ltd., Keyuan Nanlu High-Tech Zone, Chengdu, Sichuan, China (mainland).
Jian HuangDepartment of Emergency Medicine, Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu, Sichuan, China (mainland).
Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CNFourth People's Hospital of Sichuan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND This study was designed to investigate the effect of lycorine (LY) on the AMPK-mTOR-S6K signaling pathway and to clarify its role in autophagy and apoptosis. MATERIAL AND METHODS Various concentrations of LY were used to treat non-small cell lung carcinoma A549 cells. The MTT assay was used to measure cell viability and acridine orange staining was used to detect cell morphology changes. Western blot analysis was used to test the effect of LY on the expression levels of LC3, caspase 3, and other proteins involved in the AMPK-mTOR-S6K signaling pathway. RESULTS The half maximal inhibitory concentration (IC50) of LY after 24-h treatment was 8.5 μM, with stronger inhibitory effect of 24-h LY treatment over 12-h LY treatment. Morphological observation showed that lower doses (4 μM and 8 μM) of LY treatment induced A549 cell death mainly caused by autophagy, whereas the higher dose (16 μM) of LY treatment induced A549 cell death, mainly caused by apoptosis. Furthermore, 8 μM LY caused the highest conversion of LC3-II from LC3-I. All LY treatments activated caspase-3. LY treatment also promoted AMPK phosphorylation (Thr172) and inhibited the phosphorylation of mTOR and S6K. CONCLUSIONS LY induced apoptosis of A549 cells by regulating the AMPK-mTOR-S6K signaling pathway. Lower levels (4~8 μM) of LY-induced autophagy contributed to LY-induced apoptosis.

Indexed as

A549 CellsAmaryllidaceae AlkaloidsAMP-Activated Protein KinasesApoptosisAutophagyCarcinoma, Non-Small-Cell LungCaspase 3Cell Line, TumorCell ProliferationCell SurvivalHumansLung NeoplasmsMAP Kinase Signaling SystemMicrotubule-Associated ProteinsPhenanthridinesPhosphorylationAmaryllidaceae AlkaloidsAMP-Activated Protein KinasesCaspase 3lycorineMicrotubule-Associated ProteinsPhenanthridinesProto-Oncogene Proteins c-aktribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine Kinases

Identifiers

PMID28450693
PMCPMC5421746
OpenAlexW2607933002

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.