Evidence map›Paper›PMID 30275772›Full record

ArticleCancer cell international2018

Yan-Na Jiao, Li-Na Wu, Dong Xue, Xi-Juan Liu, Zhi-Hua Tian, Shan-Tong Jiang, Shu-Yan Han, Ping-Ping Li

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
5.3field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.

  1. Pooled it
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  20. Design, synthesis and anticancer activity of naphthoquinone derivatives.Journal of enzyme inhibition and medicinal chemistry · 2020
    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

8 authors at 2 institutions in 1 country.

Yan-Na Jiao *1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Integration of Chinese and Western Medicine, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142 People's Republic of China.
Li-Na Wu *2Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Central Laboratory, Peking University Cancer Hospital and Institute, Beijing, 100142 People's Republic of China.
Dong Xue *1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Integration of Chinese and Western Medicine, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142 People's Republic of China.
Xi-Juan Liu2Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Central Laboratory, Peking University Cancer Hospital and Institute, Beijing, 100142 People's Republic of China.
Zhi-Hua Tian2Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Central Laboratory, Peking University Cancer Hospital and Institute, Beijing, 100142 People's Republic of China.
Shan-Tong Jiang1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Integration of Chinese and Western Medicine, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142 People's Republic of China.
Shu-Yan Han1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Integration of Chinese and Western Medicine, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142 People's Republic of China.
Ping-Ping Li1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Integration of Chinese and Western Medicine, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing, 100142 People's Republic of China.
Peking University · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background

methodsThe proliferation of H1975 and A549 cells was evaluated by MTT assay. Cell apoptosis was assessed by Annexin V and PI staining, Caspase 3 expression and activity. Autophagy flux proteins were detected by Western blot with or without autophagy inducer and inhibitor. Endogenous LC3-II puncta and LysoTracker staining were monitored by confocal microscopy. The formation of autophagic vacuoles was measured by acridine orange staining. ERK is a crucial molecule to interplay with cell autophagy and apoptosis. The role of ERK on cell apoptosis and autophagy influenced by MTE was determined in the presence of MEK/ERK inhibitor U0126.

resultsThe significant growth inhibition and apoptosis induction were observed in MTE treated NSCLC cells. MTE induced cell apoptosis coexisted with elevated Caspase 3 activity. MTE also impaired autophagic flux by upregulated LC3-II and p62 expression. Autophagy inducer EBSS could not abolish the impaired autophagic flux by MTE, while it was augmented in the presence of autophagy inhibitor Baf A1. The autophagosome-lysosome fusion was blocked by MTE via affecting lysosome function as evidenced by decreased expression of LAMP1 and Cathepsin B. The molecule ERK became hyperactivated after MTE treatment, but the MEK/ERK inhibitor U0126 abrogated autophagy inhibition and apoptosis induction caused by MTE, suggested that ERK signaling pathways partially contributed to cell death caused by MTE.

conclusionOur results demonstrate that MTE caused apoptosis induction as well as autophagy inhibition in NSCLC cells. The activated ERK is partially associated with NSCLC apoptotic and autophagic cell death in response to MTE treatment. The present findings reveal new mechanisms for the anti-tumor activity of MTE against NSCLC.

Indexed as

ApoptosisAutophagyERK activationMarsdenia tenacissima extract (MTE)NSCLC

Identifiers

PMID30275772
PMCPMC6161462
OpenAlexW2894373686

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.