Evidence map›Paper›PMID 32724432›Full record

ArticleOncology letters2020

HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway.

Xia-Yin Zhu, Qun-Yi Guo, Min Zhu, Bao-Guo Chen, Ling-Yan Wang, Dan-Qiong Zhang, Li Zhang, Yan-Ping Shao, Wen-Da Luo

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Xia-Yin ZhuDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Qun-Yi GuoDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Min ZhuDepartment of Central Laboratory, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Bao-Guo ChenDepartment of Central Laboratory, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Ling-Yan WangDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Dan-Qiong ZhangDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Li ZhangDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Yan-Ping ShaoDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Wen-Da LuoDepartment of Hematology, Taizhou Hospital of Zhejiang, Wenzhou Medical College, Taizhou, Zhejiang 317000, P.R. China.
Wenzhou Medical University · CNZhejiang Taizhou Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myelogenous leukemia (AML) is a class of malignant tumors derived from hematopoietic stem or progenitor cells. The H2.0-like homeobox gene (HLX) encodes transcription factors that function in promoting normal hematopoietic cell proliferation and tumor immunity. The present study analyzed the effect of downregulating the HLX on cell cycle distribution and cell proliferation in AML. Moreover, the current study detected changes in the expression of genes and proteins in the Janus kinase (JAK)/STAT signaling pathway to investigate the mechanism of the action of HLX in tumor immunity in AML. HLX expression in AML cell lines was silenced using small interfering siRNA, and MTS/PMS-assay colorimetric assays were used to assess the effect of knockdown of HLX on AML cell proliferation. Flow cytometry was used to analyze changes in cell cycle distribution, while reverse transcription-quantitative PCR and western blotting were used to detect changes in the expression levels of key components of the JAK/STAT signaling pathway, such as p21-activated kinase 1 (PAK1), neuropilin 1 (NRP1), B-cell translocation gene 1 (BTG1) and STAT5. It was found that HLX was differentially expressed in AML cell lines of various subtypes, and HLX expression was higher in the AML/M3 subtype NB4 cell line compared with the control group. Knockdown of HLX in NB4 cells significantly inhibited cell proliferation and arrested cells in the G

Indexed as

HLXJanus kinase/STATNB4 cellsproliferation inhibition

Identifiers

PMID32724432
PMCPMC7377103
OpenAlexW3034271526

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.