Evidence map›Paper›PMID 31807521›Full record

ArticleAnnals of translational medicine2019

Ecliptasaponin A induces apoptosis through the activation of ASK1/JNK pathway and autophagy in human lung cancer cells.

Jia Han, Wang Lv, Hongxu Sheng, Yiqing Wang, Longxiang Cao, Sha Huang, Linhai Zhu, Jian Hu

Abstract read
In one paragraph

Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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  3. [Ecliptasaponin A ameliorates DSS-induced colitis in mice by suppressing M1 macrophage polarizationNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Jia HanDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Wang LvDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Hongxu ShengDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Yiqing WangDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Longxiang CaoDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Sha HuangDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Linhai ZhuDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Jian HuDepartment of Thoracic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is one of the causes of carcinomas mortality worldwide. Ecliptasaponin A (ES), a natural product extracted from the plant known as Eclipta prostrata, has been reported as an anti-cancer drug against various cancer cell lines. However, the exact mechanisms of ES have not yet been fully characterized.

methodsNumerous studies have been done to support that ES has a powerful inhibiting effect on the growth of cancers via the activation of apoptosis and autophagy. To explore the underlying mechanisms of anti-cancer and investigate the relationships of the apoptosis and autophagy, we used apoptosis signal-regulating kinase 1 (ASK1) inhibitor (GS-4997), c-Jun N-terminal kinase (JNK) inhibitor (SP600125), and autophagy inhibitor [chloroquine (CQ) and 3-methyladenine (3-MA)].

resultsES could potently suppress cell viability and induces apoptotic cell death of human lung cancer cells H460 and H1975. ES activated apoptosis via ASK1/JNK pathway, GS-4997 and SP600125 can attenuated these effects. Furthermore, ES could triggered autophagy in lung cancer cell lines, and the autophagy inhibitor 3-MA and CQ reversed ES-induced apoptosis in H460 and H1975 cells. Furthermore, SP600125 can inhibit autophagy.

conclusionsThis study showed that ES induces apoptosis in human lung cancer cells by triggering enhanced autophagy and ASK1/JNK pathway, which may thus be a promising agent against lung cancer.

Indexed as

apoptosisapoptosis signal-regulating kinase 1 (ASK1)autophagyc-Jun N-terminal kinase (JNK)Ecliptasaponin A (ES)Lung cancer

Identifiers

PMID31807521
PMCPMC6861768

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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.