Evidence map›Paper›PMID 26373347›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2016

Activation of Cyclic Adenosine Monophosphate Pathway Increases the Sensitivity of Cancer Cells to the Oncolytic Virus M1.

Kai Li, Haipeng Zhang, Jianguang Qiu, Yuan Lin, Jiankai Liang, Xiao Xiao, Liwu Fu, Fang Wang, Jing Cai, Yaqian Tan and 15 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed, 44 citations in OpenAlex.

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  20. RSC advances · 2020
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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

25 authors at 3 institutions in 2 countries.

Kai LiDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Haipeng ZhangDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Jianguang QiuDepartment of Urology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yuan LinDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Jiankai LiangDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Xiao XiaoDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Liwu FuState Key Laboratory for Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, China.
Fang WangState Key Laboratory for Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, China.
Jing CaiDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Yaqian TanDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Wenbo ZhuDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Wei YinDepartment of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Bingzheng LuDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Fan XingDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Lipeng TangDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Min YanDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Jialuo MaiDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Yuan LiDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Wenli ChenDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Pengxin QiuDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Xingwen SuDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Guangping GaoHorae Gene Therapy Center, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Phillip W L TaiHorae Gene Therapy Center, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Jun HuDepartment of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Guangmei YanDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CNUniversity of Massachusetts Chan Medical School · USThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncolytic virotherapy is a novel and emerging treatment modality that uses replication-competent viruses to destroy cancer cells. Although diverse cancer cell types are sensitive to oncolytic viruses, one of the major challenges of oncolytic virotherapy is that the sensitivity to oncolysis ranges among different cancer cell types. Furthermore, the underlying mechanism of action is not fully understood. Here, we report that activation of cyclic adenosine monophosphate (cAMP) signaling significantly sensitizes refractory cancer cells to alphavirus M1 in vitro, in vivo, and ex vivo. We find that activation of the cAMP signaling pathway inhibits M1-induced expression of antiviral factors in refractory cancer cells, leading to prolonged and severe endoplasmic reticulum (ER) stress, and cell apoptosis. We also demonstrate that M1-mediated oncolysis, which is enhanced by cAMP signaling, involves the factor, exchange protein directly activated by cAMP 1 (Epac1), but not the classical cAMP-dependent protein kinase A (PKA). Taken together, cAMP/Epac1 signaling pathway activation inhibits antiviral factors and improves responsiveness of refractory cancer cells to M1-mediated virotherapy.

Indexed as

AlphavirusAnimalsApoptosisCell Line, TumorColforsinCyclic AMPEndoplasmic Reticulum StressGuanine Nucleotide Exchange FactorsHCT116 CellsHumansMiceNeoplasmsOncolytic VirotherapyOncolytic VirusesSignal TransductionColforsinCyclic AMPEpac protein, mouseGuanine Nucleotide Exchange Factors

Identifiers

PMID26373347
PMCPMC4754548
OpenAlexW2261498617

What OpenQuestion holds

Textmetadata
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.