Evidence map›Paper›PMID 35117033›Full record

ArticleTranslational cancer research2019

HDAC6 inhibitor WT161 induces apoptosis in retinoblastoma cells and synergistically interacts with cisplatin.

Jun Sun, Xia Qian, Feifei Zhang, Xiaofeng Tang, Cheng Ju, Renfeng Liu, Ruihao Zhou, Zhiping Zhang, Xiao-Bin Lv, Changhua Zhang and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Histone Deacetylases in Retinoblastoma.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. HDAC6: A unique HDAC family member as a cancer target.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
  10. Article
  11. Article
  12. Article
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

11 authors at 4 institutions in 1 country.

Jun Sun *College of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang 330004, China.
Xia Qian *Nanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Feifei ZhangNanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Xiaofeng TangNanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Cheng JuNanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Renfeng LiuNanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Ruihao ZhouNanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Zhiping ZhangNanchang Key Laboratory of Orthopedics, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Xiao-Bin LvNanchang Key Laboratory of Cancer Pathogenesis and Translational Research, Center Laboratory, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Changhua ZhangCollege of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang 330004, China.
Guofu HuangDepartment of Ophthalmology, The Third Affiliated Hospital of Nanchang University, Nanchang 330008, China.
Third Hospital of Nanchang · CNNanchang University · CNJiangxi University of Traditional Chinese Medicine · CNThird Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWT161 is a recently discovered histone deacetylase 6 (HDAC6) inhibitor which shows anti-tumor effects on multiple myelomas and breast cancer. However, the role of WT161 in retinoblastoma remains unclear. The aim of this study is to explore the role of WT161 in retinoblastoma and its underlying mechanisms.

methodsThe anti-proliferation of WT161 on retinoblastoma cells was examined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and soft agar colony formation assay. Cell apoptosis was analyzed using flow cytometer. WT161 and DDP synergistic effect was evaluated by isobologram analysis using CompuSyn software.

resultsWT161 suppressed the cell growth and induced apoptosis of retinoblastoma cells in a dose- and time-dependent manner. Mechanistically, WT161 increases the transcription of Bad through activating Bad promoter. Chromatin immunoprecipitation (ChIP) assay showed WT161 treatment increased acetylated histone H3 (AcH3) and acetylated histone H4 (AcH4) on the Bad promoter in retinoblastoma cells. In addition, WT161 shows synergistically inhibitory effects on retinoblastoma cell combined with cisplatin.

conclusionsThese results indicate that WT161, as a selective HDAC6 inhibitor, is a promising agent against retinoblastoma.

Indexed as

apoptosisBadcisplatinretinoblastomasynergistic inhibitionWT161

Identifiers

PMID35117033
PMCPMC8798655
OpenAlexW2990921725

What OpenQuestion holds

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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.