Evidence map›Paper›PMID 28208579›Full record

ReviewInternational journal of molecular sciences2017

Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer.

Guangbo Liu, Fen Pei, Fengqing Yang, Lingxiao Li, Amit Dipak Amin, Songnian Liu, J Ross Buchan, William C Cho

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed, 4 pooled it
–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

221 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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161 more citing papers are in PubMed but not listed here.

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.

Guangbo LiuDepartment of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. guangboliu@email.arizona.edu.
Fen PeiDepartment of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. peifen1990@gmail.com.
Fengqing YangDepartment of Obstetrics and Gynecology, Dong'e No. 4 People's Hospital, Liaocheng 252200, China. yfqldz@gmail.com.
Lingxiao LiDepartment of Medicine, Division of Hematology-Oncology, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA. lingxiaoli@med.miami.edu.
Amit Dipak AminDepartment of Medicine, Division of Hematology-Oncology, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA. amitdipakamin@med.miami.edu.
Songnian LiuDepartment of Chemical and Life Science Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA. sliu6@vcu.edu.
J Ross BuchanDepartment of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. rbuchan@email.arizona.edu.
William C ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong, China. chocs@ha.org.hk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small-cell lung cancer (NSCLC) constitutes 85% of all lung cancers, and is the leading cause of cancer-related death worldwide. The poor prognosis and resistance to both radiation and chemotherapy warrant further investigation into the molecular mechanisms of NSCLC and the development of new, more efficacious therapeutics. The processes of autophagy and apoptosis, which induce degradation of proteins and organelles or cell death upon cellular stress, are crucial in the pathophysiology of NSCLC. The close interplay between autophagy and apoptosis through shared signaling pathways complicates our understanding of how NSCLC pathophysiology is regulated. The apoptotic effect of autophagy is controversial as both inhibitory and stimulatory effects have been reported in NSCLC. In addition, crosstalk of proteins regulating both autophagy and apoptosis exists. Here, we review the recent advances of the relationship between autophagy and apoptosis in NSCLC, aiming to provide few insights into the discovery of novel pathogenic factors and the development of new cancer therapeutics.

Indexed as

ApoptosisAutophagyAnimalsApoptosis Regulatory ProteinsCarcinoma, Non-Small-Cell LungCell CommunicationEndoplasmic Reticulum StressEnergy MetabolismGenetic VariationHumansImmunotherapyLung NeoplasmsMAP Kinase Signaling SystemMolecular Targeted TherapyProtein BindingRisk FactorsApoptosis Regulatory ProteinsTOR Serine-Threonine Kinasesapoptosisautophagycrosstalkendoplasmic reticulum (ER) stressmammalian target of rapamycin (mTOR)non-small-cell lung cancer (NSCLC)p53

Identifiers

PMID28208579
PMCPMC5343902

What OpenQuestion holds

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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.