Evidence map›Paper›PMID 31217472›Full record

ArticleCell death & disease2019

LZ-101, a novel derivative of danofloxacin, induces mitochondrial apoptosis by stabilizing FOXO3a via blocking autophagy flux in NSCLC cells.

Yongjian Guo, Yue Zhao, Yuxin Zhou, Xiaoqing Tang, Zhiyu Li, Xiaotang Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. 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
0.9field-weighted citation impact, top 26% 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, 19 citations in OpenAlex.

  1. Article
  2. Review
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  8. [Role of autophagy in lipopolysaccharide-induced apoptosis of odontoblasts].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    Article
  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

6 authors at 3 institutions in 2 countries.

Yongjian GuoDepartment of Chemistry and Biochemistry, Florida International University, Miami, FL, USA.
Yue ZhaoState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, 210009, Nanjing, The People's Republic of China.
Yuxin ZhouState Key Laboratory of Natural Medicines, Jiangsu Key Laboratory of Carcinogenesis and Intervention, China Pharmaceutical University, 24 Tongjiaxiang, 210009, Nanjing, The People's Republic of China.
Xiaoqing TangDepartment of Chemistry and Biochemistry, Florida International University, Miami, FL, USA.
Zhiyu LiState Key Laboratory of Natural Medicines, Department of Natural Medicinal Chemistry, China Pharmaceutical University, 24 Tongjiaxiang, 210009, Nanjing, The People's Republic of China.
Xiaotang WangDepartment of Chemistry and Biochemistry, Florida International University, Miami, FL, USA. wangx@fiu.edu.
Florida International University · USChina Pharmaceutical University · CNState Key Laboratory of Natural Medicine

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small-cell lung carcinoma (NSCLC) continues to be a vital disease worldwide for its high incidence and consequent mortality rate. In this study, we investigated the anti-cancer effect of LZ-101, a new derivative of danofloxacin, against non-small-cell lung cancer and the underlying mechanisms. In vitro, LZ-101 inhibited the viability of human non-small cell lung cancer cell lines. We demonstrated that LZ-101 induced mitochondrial-mediated apoptosis by increasing Bax/Bcl-2 ratio, loss of mitochondrial membrane potential (ΔΨm), release of cytochrome c (Cyt c) and apoptosis-inducing factor (AIF) in A549 cells. Further research illuminated that LZ-101 induced apoptosis was related to the activation of FOXO3a/Bim pathway. Moreover, we found that LZ-101 increased the stability of FOXO3a by blocking autophagy-dependent FOXO3a degradation. However, inhibition of autophagosome formation abolished FOXO3a stabilization and apoptosis induced by LZ-101. In vivo, LZ-101 exerted a remarkable anti-tumor activity with high safety in xenograft model inoculated A549 tumor through the same mechanism as in our in vitro study. In conclusion, our findings indicated that LZ-101 induces mitochondrial apoptosis and stabilizes FOXO3a by blocking autophagy flux.

Indexed as

A549 CellsAnimalsAnti-Infective AgentsAntineoplastic AgentsApoptosisAutophagyCarcinoma, Non-Small-Cell LungCell Line, TumorCell SurvivalFluoroquinolonesForkhead Box Protein O3HumansLung NeoplasmsMaleMiceMice, Inbred BALB CAnti-Infective AgentsAntineoplastic AgentsdanofloxacinFluoroquinolonesForkhead Box Protein O3Proteasome Endopeptidase Complex

Identifiers

PMID31217472
PMCPMC6584698
OpenAlexW2952568004

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.