Evidence map›Paper›PMID 31831854›Full record

ArticleCancer gene therapy2020

The role of phosphorylation of MLF2 at serine 24 in BCR-ABL leukemogenesis.

Juhua Yang, Donglin Cao, Yanrong Zhang, Ruiming Ou, Zhao Yin, Yanjun Liu, Guiping Huang, Chunming Gu, Shengting Chen, Jia Fei

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. First Glance at Myeloid Leukaemia Factor 2 in Cardiomyocytes.Journal of cardiovascular development and disease · 2025
    Article
  2. Article
  3. Article
  4. MLF2 Negatively Regulates P53 and Promotes Colorectal Carcinogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  5. Article
  6. 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 4 institutions in 1 country.

Juhua Yang *Department of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, 510632, China.
Donglin Cao *Department of Laboratory Medicine, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Yanrong Zhang *Department of Hematology, The First Affiliated Hospital of Jinan University, Guangzhou, 510317, China.
Ruiming OuDepartment of Hematology, Guangdong Second Provincial General Hospital, Guangzhou, 510317, China.
Zhao YinDepartment of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, 510632, China.ORCID http://orcid.org/0000-0002-3404-8446
Yanjun LiuDepartment of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, 510632, China.
Guiping HuangDepartment of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, 510632, China.
Chunming GuDepartment of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, 510632, China.
Shengting ChenDepartment of Hematology, The First Affiliated Hospital of Jinan University, Guangzhou, 510317, China.
Jia FeiDepartment of Biochemistry and Molecular Biology, Medical College of Jinan University, Guangzhou, 510632, China. tfeijia@jnu.edu.cn.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CNGuangdong Provincial People's Hospital · CNGuangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic myelogenous leukemia (CML) is a myeloproliferative disorder defined by the presence of the fusion gene BCR-ABL1 in primitive hematopoietic progenitors. The myeloid leukemia factors (MLFs) were identified in the fly and human, and are involved in acute leukemia and enhancing the myeloid factor; however, the function of MLF2 in CML is poorly understood. In this study, we demonstrated that MLF2 may play an oncogenic role in CML. The expression level of MLF2 was related to the proliferation, colony-formation ability, and sensitivity to imatinib in K562 cells. Moreover, phosphorylation at serine 24, detected through Phos-tag sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was required to maintain the activity of MLF2 in CML. The effects of MLF2 overexpression on the colony-formation ability in vitro and mouse survival in vivo could be alleviated by point mutation of MLF2 at serine 24. These findings uncover the oncogenic role of MLF2 through phosphorylation at serine 24 and provide a novel therapeutic target in CML.

Indexed as

Gene Expression Regulation, LeukemicAnimalsApoptosisCarcinogenesisCell ProliferationColony-Forming Units AssayDrug Resistance, NeoplasmFusion Proteins, bcr-ablGene Knockdown TechniquesHumansImatinib MesylateK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMiceNeoplastic Stem CellsNuclear ProteinsBCR-ABL1 fusion protein, humanFusion Proteins, bcr-ablImatinib MesylateMLF2 protein, humanNuclear ProteinsProtein Kinase InhibitorsRNA, Small InterferingSerine

Identifiers

PMID31831854
OpenAlexW2996363730

What OpenQuestion holds

Textmetadata
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.