Evidence map›Paper›PMID 35667090›Full record

ArticleBlood advances2022

Upregulated SPAG6 promotes acute myeloid leukemia progression through MYO1D that regulates the EGFR family expression.

Jiao Mu, Peng Yuan, Jie Luo, Yafan Chen, Yiyuan Tian, Li Ding, Beibei Zhao, Xiaocheng Wang, Bao Wang, Lin Liu

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. MUC13-Associated Molecular Interactome in Pancreatic Cancer.Computational and structural biotechnology journal · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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

10 authors at 7 institutions in 2 countries.

Jiao MuDepartment of Hematology, and.
Peng YuanDepartment of Interventional Radiology and Pain Treatment, Tangdu Hospital, Air Force Medical University, Xi'an, China.
Jie LuoDepartment of Hematology, and.
Yafan ChenDepartment of Human Movement Science, Xi'an Physical Education University, Xi'an, China.
Yiyuan TianDepartment of Physiology, Medical College of Yan'an University, Yan'an, China; and.
Li DingDepartment of Hematology, and.
Beibei ZhaoDepartment of Hematology, and.
Xiaocheng WangCenter of Clinical Aerospace Medicine, School of Aerospace Medicine, Key Laboratory of Aerospace Medicine of Ministry of Education.
Bao WangTangdu Hospital, Department of Neurosurgery, Air Force Medical University, Xi'an, China.
Lin LiuDepartment of Hematology, and.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNInstitute of Aviation Medicine · CZPeople 's Liberation Army 451 Hospital · CNTang Du Hospital · CNXi'an Physical Education University · CNYan'an University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal aberrations and gene mutations have been considered to be the major reasons for high recurrence rates and poor survival among acute myeloid leukemia (AML) patients. However, the underlying molecular mechanism of AML gene mutation remains largely unclear. Here, we show that SPAG6 (sperm-associated antigen 6), one of the most markedly increased SPAG genes in AML, significantly contributed to the proliferation and migration of leukemic cells. SPAG6 was highly expressed in AML, and its upregulation was negatively correlated with the prognosis of the disease. In vitro, SPAG6 promoted the proliferation and migration of leukemia cells and promoted cell cycle progression from the G1 phase to the S phase. In vivo, low expression of SPAG6 reduced the proliferation and infiltration of leukemia cells and prolonged the survival of xenograft tumor mice. Furthermore, immunoprecipitation and mass spectrometry analysis showed that SPAG6 interacts with MYO1D (myosin 1D). Specifically, overexpression of SPAG6 promoted the translocation of MYO1D into the cell membrane, thus upgrading the expression level of the EGFR family and thereby promoting the progression of AML. Overall, our study found that SPAG6 combined with MYO1D and translocated MYO1D from the cytosol to the cytomembrane, which induced the PI3K (phosphoinositide 3-kinase)/AKT (protein kinase B) signaling and ERK (extracellular signal-regulated kinase) signaling pathway to regulate the growth and prognosis of AML. SPAG6 may become a new target gene for the treatment of AML.

Indexed as

Leukemia, Myeloid, AcuteProto-Oncogene Proteins c-aktAnimalsCell ProliferationErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHumansMiceMicrotubule ProteinsMyosinsPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesEGFR protein, humanErbB ReceptorsExtracellular Signal-Regulated MAP KinasesMicrotubule ProteinsMyo1d protein, mouseMyosinsPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSPAG6 protein, humanSPAG6 protein, mouse

Identifiers

PMID35667090
PMCPMC9631693
OpenAlexW4282025543

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.