Evidence map›Paper›PMID 27811372›Full record

ArticleOncotarget2016

The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex.

Lanmei Chen, Guodong Li, Fa Peng, Xinming Jie, Guangzhi Dongye, Kangrong Cai, Ruibing Feng, Baojun Li, Qingwang Zeng, Kaiyi Lun and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 59 citations in OpenAlex.

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  6. Cyclometalated Ru(II) β-carboline complexes induce cell cycle arrest and apoptosis in human HeLa cervical cancer cells via suppressing ERK and Akt signaling.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2021
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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

12 authors at 2 institutions in 2 countries.

Lanmei ChenSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Guodong LiSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Fa PengSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Xinming JieAnalysis Centre of Guangdong Medical University, Zhanjiang, 524023, China.
Guangzhi DongyeAnalysis Centre of Guangdong Medical University, Zhanjiang, 524023, China.
Kangrong CaiAnalysis Centre of Guangdong Medical University, Zhanjiang, 524023, China.
Ruibing FengState Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau, 999078, China.
Baojun LiSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Qingwang ZengSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Kaiyi LunSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Jincan ChenAnalysis Centre of Guangdong Medical University, Zhanjiang, 524023, China.
Bilian XuSchool of Pharmacy, Guangdong Medical University, Zhanjiang, 524023, China.
Guangdong Medical College · CNUniversity of Macau · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study, it was found that the ruthenium (II) imidazole complex [Ru(Im)4(dppz)]2+ (Ru1) could induce significant growth inhibition and apoptosis in A549 and NCI-H460 cells. Apart from the induction of apoptosis, it was reported for the first time that Ru1 induced an autophagic response in A549 and NCI-H460 cells as evidenced by the formation of autophagosomes, acidic vesicular organelles (AVOs), and the up-regulation of LC3-II. Furthermore, scavenging of reactive oxygen species (ROS) by antioxidant NAC or Tiron inhibited the release of cytochrome c, caspase-3 activity, and eventually rescued cancer cells from Ru1-mediated apoptosis, suggesting that Ru1 inducing apoptosis was partially caspase 3-dependent by triggering ROS-mediated mitochondrial dysfunction in A549 and NCI-H460 cells. Further study indicated that the extracellular signal-regulated kinase (ERK) signaling pathway was involved in Ru1-induced autophagy in A549 and NCI-H460 cells. Moreover, blocking autophagy using pharmacological inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) enhanced Ru1-induced apoptosis, indicating the cytoprotective role of autophagy in Ru1-treated A549 and NCI-H460 cells. Finally, the in vivo mice bearing A549 xenografts, Ru1 dosed at 10 or 20 mg/kg significantly inhibited tumor growth.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsApoptosisAutophagosomesAutophagyCaspase 3Cell Cycle CheckpointsCell ProliferationCytochromes cDose-Response Relationship, DrugExtracellular Signal-Regulated MAP KinasesFemaleHumansImidazolesLung NeoplasmsAntineoplastic AgentsCASP3 protein, humanCaspase 3Cytochromes cExtracellular Signal-Regulated MAP KinasesImidazolesMAP1LC3A protein, humanMicrotubule-Associated ProteinsOrganometallic CompoundsReactive Oxygen SpeciesRutheniumapoptosisautophagycytotoxicityreactive oxygen speciesruthenium imidazole complex

Identifiers

PMID27811372
PMCPMC5348350
OpenAlexW2548261792

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.