Evidence map›Paper›PMID 28098170›Full record

ArticleScientific reports2017

Targeting the PI3K/AKT pathway via GLI1 inhibition enhanced the drug sensitivity of acute myeloid leukemia cells.

Hui Liang, Qi-Li Zheng, Peng Fang, Jian Zhang, Tuo Zhang, Wei Liu, Min Guo, Christopher L Robinson, Shui-Bing Chen, Xiao-Ping Chen and 2 more

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

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. High GLI-1 Expression is a Reliable Indicator of Bad Prognosis in Newly Diagnosed Acute Leukemia Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023
    Article
  5. Review
  6. Article
  7. MiR-140 Targets lncRNA DNAJC3-AS1 to Suppress Cell Proliferation in Acute Myeloid Leukemia.Mediterranean journal of hematology and infectious diseases · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. 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

12 authors at 3 institutions in 2 countries.

Hui LiangDepartment of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Qi-Li ZhengDepartment of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Peng FangDepartment of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jian ZhangDepartment of Hematology, Third Xiangya Hospital, Central South University, China.
Tuo ZhangGenomic Core, Weill Cornell Medical College, NY, USA.
Wei LiuDepartment of Oncology, Xiangya Hospital, Central South University, China.
Min GuoDepartment of Endocrinology, Xiangya Hospital, Central South University, China.
Christopher L RobinsonDepartment of Surgery Genomic Core, Weill Cornell Medical College, NY, USA.
Shui-Bing ChenDepartment of Surgery Genomic Core, Weill Cornell Medical College, NY, USA.
Xiao-Ping ChenDepartment of Clinical Pharmacology, Xiangya Hospital, Central South University, China.
Fang-Ping ChenDepartment of Hematology, Third Xiangya Hospital, Central South University, China.
Hui ZengDepartment of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Central South University · CNCornell University · USXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Combination targeted therapy is commonly used to treat acute myeloid leukemia (AML) patients, particularly in refractory/relapse (RR) population. However, concerns have been raised regarding the safety and patient tolerance of combination chemotherapy. It is critical to choose the appropriate treatment for precision therapy. We performed genome-wide RNA profiling using RNA-Seq to compare the RR group and the complete remission (CR) group (a total of 42 adult AML patients). The Hedgehog (Hh) and PI3K/AKT pathways were upregulated in the RR population, which was further confirmed by western blot and/or qPCR. Overexpression of GLI1 in AML cells led to increased AKT phosphorylation and decreased drug sensitivity, which was attenuated by GLI1 inhibition. By contrast, neither the expression of GLI1 nor apoptosis in response to Ara-C treatment of AML cells was significantly affected by PI3K inhibition. Furthermore, co-inhibition of GLI1 and PI3K induced apoptosis of hematopoietic stem/progenitor cells (HSPCs), which raised serious concerns about the side effects of this treatment. These results indicated that GLI1 inhibition alone, but not combined inhibition, is sufficient to enhance AML drug sensitivity, which provides a novel therapeutic strategy for AML treatment.

Indexed as

Molecular Targeted TherapyAdultApoptosisCell Line, TumorCell ProliferationFemaleGene Expression Regulation, LeukemicHumansLeukemia, Myeloid, AcuteMaleMiddle AgedNeoplasm Recurrence, LocalPhosphatidylinositol 3-KinasesPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-aktGLI1 protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktZinc Finger Protein GLI1

Identifiers

PMID28098170
PMCPMC5241777
OpenAlexW2578154236

What OpenQuestion holds

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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.