Evidence map›Paper›PMID 26329846›Full record

ArticleScientific reports2015

SC06, a novel small molecule compound, displays preclinical activity against multiple myeloma by disrupting the mTOR signaling pathway.

Kunkun Han, Xin Xu, Zhuan Xu, Guodong Chen, Yuanying Zeng, Zubin Zhang, Biyin Cao, Yan Kong, Xiaowen Tang, Xinliang Mao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 21 citations in OpenAlex.

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  16. Multiple myeloma in the marrow: pathogenesis and treatments.Annals of the New York Academy of Sciences · 2016
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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 2 institutions in 1 country.

Kunkun HanJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Xin XuJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Zhuan XuDepartment of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Guodong ChenJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Yuanying ZengJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Zubin ZhangJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Biyin CaoJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Yan KongDepartment of Neurology, The First Affiliated Hospital of Soochow University, Suzhou, China.
Xiaowen TangDepartment of Hematology, the First Affiliated Hospital of Soochow University, Suzhou, China.
Xinliang MaoJiangsu Key Laboratory of Translational Research and Therapy for Neuro-psycho-diseases, Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
Soochow University · CNFirst Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian target of rapamycin (mTOR) is extensively involved in multiple myeloma (MM) pathophysiology. In the present study, we reported a novel small molecule SC06 that induced MM cell apoptosis and delayed MM xenograft growth in vivo. Oral administration of SC06 to mice bearing human MM xenografts resulted in significant inhibition of tumor growth at doses that were well tolerated. Mechanistic studies revealed that SC06 selectively inhibited the mTOR signaling pathway but had no effects on other associated kinases, such as AKT, ERK, p38, c-Src and JNK. Further studies showed that SC06-decreased mTOR activation was associated with the downregulation of Raptor, a key component of the mTORC1 complex. SC06 also suppressed the phosphorylation of 4E-BP1 and P70S6K, two typical substrates in the mTORC1 signaling pathway. Notably, expression of Raptor, phosphorylation of mTOR and phosphorylated 4E-BP1 was also decreased in the tumor tissues from SC06-treated mice, which was consistent with the cellular studies. Therefore, given the potency and low toxicity, SC06 could be developed as a potential anti-MM drug candidate by disrupting the mTOR signaling.

Indexed as

Adaptor Proteins, Signal TransducingAminopyridinesAnimalsApoptosisCell Line, TumorCell SurvivalDown-RegulationFemaleHEK293 CellsHumansHydrazonesLysosomesMechanistic Target of Rapamycin Complex 1Mice, NudeMultiple MyelomaMultiprotein Complexes3-chloro-2-(2-((1-(4-(trifluoromethoxy)phenyl)-1H-pyrrol-2-yl)methylene)hydrazinyc)-5-(trifluoromethyl)pyridineAdaptor Proteins, Signal TransducingAminopyridinesHydrazonesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProteasome Endopeptidase ComplexRegulatory-Associated Protein of mTORRPTOR protein, humanSmall Molecule LibrariesTOR Serine-Threonine Kinases

Identifiers

PMID26329846
PMCPMC4556980
OpenAlexW2417413830

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.