Evidence map›Paper›PMID 29513749›Full record

ArticlePloS one2018

Chloroquine augments TRAIL-induced apoptosis and induces G2/M phase arrest in human pancreatic cancer cells.

Hiroyuki Monma, Yuichi Iida, Tamami Moritani, Tamio Okimoto, Ryosuke Tanino, Yoshitsugu Tajima, Mamoru Harada

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 38 citations in OpenAlex.

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  7. Chloroquine commonly induces hormetic dose responses.The Science of the total environment · 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

7 authors at 1 institution in 1 country.

Hiroyuki MonmaDepartment of Digestive and General Surgery, Shimane University Faculty of Medicine, Shimane, Japan.
Yuichi IidaDepartment of Immunology, Shimane University Faculty of Medicine, Shimane, Japan.
Tamami MoritaniDepartment of Immunology, Shimane University Faculty of Medicine, Shimane, Japan.
Tamio OkimotoDivision of Medical Oncology & Respiratory Medicine, Department of Internal Medicine, Shimane University Faculty of Medicine, Shimane, Japan.
Ryosuke TaninoDivision of Medical Oncology & Respiratory Medicine, Department of Internal Medicine, Shimane University Faculty of Medicine, Shimane, Japan.
Yoshitsugu TajimaDepartment of Digestive and General Surgery, Shimane University Faculty of Medicine, Shimane, Japan.
Mamoru HaradaDepartment of Immunology, Shimane University Faculty of Medicine, Shimane, Japan.ORCID 0000-0002-9737-0360
Shimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy contributes to the treatment-resistance of many types of cancers, and chloroquine (CQ) inhibits autophagy. The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) kills cancer cells but is minimally cytotoxic to normal cells. However, because the therapeutic efficacy of TRAIL is limited, it is necessary to augment TRAIL-induced anti-tumor effects. In this study, we explored the anti-tumor effects of a combination of CQ and TRAIL on two human pancreatic cancer cell lines: TRAIL-sensitive MiaPaCa-2 cells and Panc-1 cells that are less sensitive to TRAIL. Although both CQ and TRAIL reduced cancer cell viability in a dose-dependent manner, the combination acted synergistically. CQ increased the expression level of type-II LC3B without decreasing the expression of p62, an autophagic substrate, thus indicating inhibition of autophagy. CQ did not increase the levels of death receptors on cancer cells but reduced the expression of anti-apoptotic proteins. A combination of CQ and TRAIL significantly increased cancer cell apoptosis. CQ induced cell-cycle arrest in the G2/M phase. Also, CQ increased the p21 level but reduced that of cyclin B1. A combination of CQ and TRAIL reduced the colony-forming abilities of cancer cells to extents greater than either material alone. In xenograft models, combination CQ and TRAIL therapy significantly suppressed the growth of subcutaneously established MiaPaCa-2 and Panc-1 cells, compared with the untreated or monotherapy groups. Together, the results indicate that CQ in combination with TRAIL may be useful to treat human pancreatic cancer.

Indexed as

G2 Phase Cell Cycle CheckpointsAnimalsApoptosisApoptosis Regulatory ProteinsAutophagyCell Line, TumorChloroquineDrug SynergismFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB CMice, NudePancreatic NeoplasmsSpecific Pathogen-Free OrganismsApoptosis Regulatory ProteinsChloroquineTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID29513749
PMCPMC5841811
OpenAlexW2790006183

What OpenQuestion holds

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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.