Evidence map›Paper›PMID 28184925›Full record

ArticleOncology reports2017

Inhibiting PLK1 induces autophagy of acute myeloid leukemia cells via mammalian target of rapamycin pathway dephosphorylation.

Yan-Fang Tao, Zhi-Heng Li, Wei-Wei Du, Li-Xiao Xu, Jun-Li Ren, Xiao-Lu Li, Fang Fang, Yi Xie, Mei Li, Guang-Hui Qian and 10 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. PLK1 inhibition impairs erythroid differentiation.Frontiers in cell and developmental biology · 2024
    Article
  6. Article
  7. Review
  8. Review
  9. Rigosertib and Cholangiocarcinoma: A Cell Cycle Affair.International journal of molecular sciences · 2021
    Article
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  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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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

20 authors at 1 institution in 1 country.

Yan-Fang TaoInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Zhi-Heng LiInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Wei-Wei DuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Li-Xiao XuInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Jun-Li RenDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Xiao-Lu LiInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Fang FangInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Yi XieInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Mei LiInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Guang-Hui QianInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Yan-Hong LiInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Yi-Ping LiInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Gang LiInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Yi WuInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Xing FengInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Jian WangInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Wei-Qi HeCAM-SU Genomic Resource Center, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Shao-Yan HuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Jun LuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Jian PanInstitute of Pediatrics, Children's Hospital of Soochow University, Suzhou, Jiangsu 215003, P.R. China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Decreased autophagy is accompanied by the development of a myeloproliferative state or acute myeloid leukemia (AML). AML cells are often sensitive to autophagy‑inducing stimuli, prompting the idea that targeting autophagy can be useful in AML cytotoxic therapy. AML NB4 cells overexpressing microtubule-associated protein 1 light chain 3-green fluorescent protein were screened with 69 inhibitors to analyze autophagy activity. AML cells were treated with the polo-like kinase 1 (PLK1) inhibitors RO3280 and BI2536 before autophagy analysis. Cleaved LC3 (LC3-II) and the phosphorylation of mammalian target of rapamycin (mTOR), adenosine monophosphate-activated protein kinase, and Unc-51-like kinase 1 during autophagy was detected with western blotting. Autophagosomes were detected using transmission electron microscopy. Several inhibitors had promising autophagy inducer effects: BI2536, MLN0905, SK1-I, SBE13 HCL and RO3280. Moreover, these inhibitors all targeted PLK1. Autophagy activity was increased in the NB4 cells treated with RO3280 and BI2536. Inhibition of PLK1 expression in NB4, K562 and HL-60 leukemia cells with RNA interference increased LC3-II and autophagy activity. The phosphorylation of mTOR was reduced significantly in NB4 cells treated with RO3280 and BI2536, and was also reduced significantly when PLK1 expression was downregulated in the NB4, K562 and HL-60 cells. We demonstrate that PLK1 inhibition induces AML cell autophagy and that it results in mTOR dephosphorylation. These results may provide new insights into the molecular mechanism of PLK1 in regulating autophagy.

Indexed as

AutophagyAnimalsBiomarkers, TumorBlotting, WesternCell Cycle ProteinsCell ProliferationChildFemaleHumansLeukemia, Myeloid, AcuteMaleMiceNeoplasm StagingPhosphorylationPolo-Like Kinase 1PrognosisBiomarkers, TumorCell Cycle ProteinsMTOR protein, humanPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsRNA, MessengerRNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID28184925
PMCPMC5364848
OpenAlexW2584518172

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.