Evidence map›Paper›PMID 25884180›Full record

ArticleBMC cancer2015

Tenovin-6-mediated inhibition of SIRT1/2 induces apoptosis in acute lymphoblastic leukemia (ALL) cells and eliminates ALL stem/progenitor cells.

Yanli Jin, Qi Cao, Chun Chen, Xin Du, Bei Jin, Jingxuan Pan

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-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

30 citing papers in PubMed, 42 citations in OpenAlex.

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  12. Comprehensive analysis ofFrontiers in genetics · 2022
    Article
  13. Trending topics of SIRT1 in tumorigenicity.Biochimica et biophysica acta. General subjects · 2021
    Review
  14. Review
  15. Article
  16. Article
  17. The Versatility of Sirtuin-1 in Endocrinology and Immunology.Frontiers in cell and developmental biology · 2020
    Review
  18. Article
  19. Article
  20. Role of SIRT1 in hematologic malignancies.Journal of Zhejiang University. Science. B · 2019
    Review
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

6 authors at 3 institutions in 1 country.

Yanli JinDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China. yanlijin2014@163.com.
Qi CaoDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China. Caodapi@163.com.
Chun ChenDepartment of Pediatrics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510000, People's Republic of China. chenchun69@126.com.
Xin DuDepartment of Hematology, Guangdong Provincial People's Hospital, Guangzhou, 510080, People's Republic of China. miyadu@hotmail.com.
Bei JinDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China. jinbei@mail2.sysu.edu.cn.
Jingxuan PanDepartment of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, People's Republic of China. panjx2@mail.sysu.edu.cn.
Sun Yat-sen University · CNGuangdong Provincial People's Hospital · CNSun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute lymphoblastic leukemia (ALL) is a heterogeneous group of malignant disorders derived from B- or T-cell lymphoid progenitor cells. ALL often is refractory to or relapses after treatment; thus, novel targeted therapy for ALL is urgently needed. In the present study, we initially found that the level of SIRT1, a class III histone deacetylase, was higher in primary ALL cells from patients than in peripheral blood mononuclear cells from healthy individuals. But it is not clear whether inhibition of SIRT1 by its selective small molecule inhibitor Tenovin-6 is effective against ALL cells.

methodsWe tested the effect of Tenovin-6 on ALL cell lines (REH and NALM-6) and primary cells from 41 children with ALL and 2 adult patients with ALL. The effects of Tenovin-6 on cell viability were determined by MTS assay; colony-forming assays were determined by soft agar in ALL cell lines and methylcellulose medium in normal bone marrow cells and primary ALL blast cells; cell apoptosis and cell cycling were examined by flow cytometry; the signaling pathway was determined by Western blotting; ALL stem/progenitor cells were seperated by using MACS MicroBead kit.

resultsThe results showed that Tenovin-6 treatment activated p53, potently inhibited the growth of pre-B ALL cells and primary ALL cells, and sensitized ALL cells to frontline chemotherapeutic agents etoposide and cytarabine. Tenovin-6 induced apoptosis in REH and NALM-6 cells and primary ALL cells and diminished expression of Mcl-1 and X-linked inhibitor of apoptosis protein (XIAP) in such cells. Furthermore, inhibition of SIRT1 by Tenovin-6 inhibited the Wnt/β-catenin signaling pathway and eliminated ALL stem/progenitor (CD133 + CD19-) cells.

conclusionOur results indicate that Tenovin-6 may be a promising targeted therapy for ALL and clinical trials are warranted to investigate its efficacy in ALL patients.

Indexed as

AcetylationAdolescentAdultAntineoplastic AgentsApoptosisBenzamidesCell CycleCell Line, TumorCell ProliferationCell SurvivalChildChild, PreschoolFemaleHumansInfantMaleAntineoplastic AgentsBenzamidesSirtuin 1Sirtuin 2tenovin-6Tumor Suppressor Protein p53

Identifiers

PMID25884180
PMCPMC4394409
OpenAlexW2035405658

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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.