Evidence map›Paper›PMID 27552933›Full record

ArticleScientific reports2016

Combined expression of miR-34a and Smac mediated by oncolytic vaccinia virus synergistically promote anti-tumor effects in Multiple Myeloma.

Wen Lei, Shibing Wang, Chunmei Yang, Xianbo Huang, Zhenzhen Chen, Wei He, Jianping Shen, Xinyuan Liu, Wenbin Qian

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  12. Oncolytic Virotherapy and Microenvironment in Multiple Myeloma.International journal of molecular sciences · 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

9 authors at 4 institutions in 1 country.

Wen LeiInstitute of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, P.R. China.
Shibing WangClinical Research Institute, Zhejiang Provincial People's Hospital, Hangzhou, 310014, P.R. China.
Chunmei YangInstitute of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, P.R. China.
Xianbo HuangInstitute of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, P.R. China.
Zhenzhen ChenInstitute of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, P.R. China.
Wei HeInstitute of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, P.R. China.
Jianping ShenDepartment of Hematology, the First Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, 310006, P.R. China.
Xinyuan LiuInstitute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, 200031, P.R. China.
Wenbin QianInstitute of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, P.R. China.
Zhejiang University · CNChinese Academy of Sciences · CNZhejiang Chinese Medical University · CNZhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite great progress made in the treatment of multiple myeloma (MM), it is still incurable. Promising phase II clinical results have been reported recently for oncolytic vaccinia virus (OVV) clinic therapeutics. One reason for this has focused on the critical therapeutic importance of the immune response raised by these viruses. However, few studies have performed their applications as an optimal delivery system for therapeutic gene, especially miRNA in MM. In this study, we constructed two novel OVVs (TK deletion) that express anti-tumor genes, miR-34a and Smac, respectively, in MM cell lines and xenograft model. The results demonstrated that the novel OVV can effectively infect MM cell lines, and forcefully enhance the exogenous gene (miR-34a or Smac) expression. Furthermore, utilization of VV-miR-34a combined with VV-Smac synergistically inhibited tumor growth and induced apoptosis in vitro and in vivo. The underlying mechanism is proposed that blocking of Bcl-2 by VV-miR-34a increases the release of cytochrome c from mitochondria and then synergistically amplifies the antitumor effects of Smac-induced cell apoptosis. Our study is the first to utilize OVV as the vector for miR-34a or Smac expression to treat MM, and lays the groundwork for future clinical therapy for MM.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCell Line, TumorCytochromes cFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMice, Inbred BALB CMicroRNAsMitochondriaMitochondrial ProteinsMultiple MyelomaOncolytic VirotherapyOncolytic VirusesApoptosis Regulatory ProteinsCytochromes cDIABLO protein, humanIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN34 microRNA, humanMitochondrial Proteins

Identifiers

PMID27552933
PMCPMC5001249
OpenAlexW2510155489

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.