Evidence map›Paper›PMID 28440486›Full record

ArticleMolecular medicine reports2017

Synergistic antitumor effects of CDK inhibitor SNS‑032 and an oncolytic adenovirus co‑expressing TRAIL and Smac in pancreatic cancer.

Yun Ge, Wen Lei, Yingyu Ma, Yigang Wang, Buyun Wei, Xiaoyi Chen, Guoqing Ru, Xianglei He, Xiaozhou Mou, Shibing Wang

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

Article in Molecular medicine reports, 2017. 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
1.8field-weighted citation impact, top 14% 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, 20 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Yun GeXinyuan Institute of Medicine and Biotechnology, College of Life Sciences, Zhejiang Sci‑Tech University, Hangzhou, Zhejiang 310018, P.R. China.
Wen LeiDepartment of Hematology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Yingyu MaClinical Research Institute, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
Yigang WangXinyuan Institute of Medicine and Biotechnology, College of Life Sciences, Zhejiang Sci‑Tech University, Hangzhou, Zhejiang 310018, P.R. China.
Buyun WeiXinyuan Institute of Medicine and Biotechnology, College of Life Sciences, Zhejiang Sci‑Tech University, Hangzhou, Zhejiang 310018, P.R. China.
Xiaoyi ChenClinical Research Institute, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
Guoqing RuDepartment of Pathology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
Xianglei HeDepartment of Pathology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
Xiaozhou MouClinical Research Institute, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
Shibing WangClinical Research Institute, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China.
Zhejiang Provincial People's Hospital · CNZhejiang Sci-Tech University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gene therapy using oncolytic adenoviruses is a novel approach for human cancer therapeutics. The current study aimed to investigate whether the combined use of an adenovirus expressing tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL) and second mitochondria‑derived activator of caspase (Smac) upon caspase activation (ZD55‑TRAIL‑IETD‑Smac) and cyclin‑dependent kinase (CDK) inhibitor SNS‑032 will synergistically reinforce their anti‑pancreatic cancer activities. The experiments in vitro demonstrated that SNS‑032 enhances ZD55‑TRAIL‑IETD‑Smac‑induced apoptosis and causes marked pancreatic cancer cell death. Western blot assays suggested that the SNS‑032 intensified ZD55‑TRAIL‑IETD‑Smac‑induced apoptosis of pancreatic cancer cells by affecting anti‑apoptotic signaling elements, including CDK‑2, CDK‑9, Mcl‑1 and XIAP. Additionally, animal experiments further confirmed that the combination of SNS‑032 and ZD55‑TRAIL‑IETD‑Smac significantly inhibited the growth of BxPC‑3 pancreatic tumor xenografts. In conclusion, the present study demonstrated that SNS‑032 sensitizes human pancreatic cancer cells to ZD55‑TRAIL‑IETD‑Smac‑induced cell death in vitro and in vivo. These findings indicate that combined treatment with SNS‑032 and ZD55‑TRAIL‑IETD‑Smac could represent a rational approach for anti‑pancreatic cancer therapy.

Indexed as

Oncolytic VirotherapyAdenoviridaeAnimalsApoptosisApoptosis Regulatory ProteinsCell Cycle CheckpointsCell Line, TumorCombined Modality TherapyDisease Models, AnimalGene ExpressionGenetic TherapyGenetic VectorsHumansIntracellular Signaling Peptides and ProteinsMaleMiceApoptosis Regulatory ProteinsDIABLO protein, humanIntracellular Signaling Peptides and ProteinsMitochondrial ProteinsN-(5-(((5-(1,1-dimethylethyl)-2-oxazolyl)methyl)thio)-2-thiazolyl)-4-piperidinecarboxamideOxazolesThiazolesTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID28440486
PMCPMC5436152
OpenAlexW2606334292

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.