Evidence map›Paper›PMID 39307938›Full record

ArticleCancer reports (Hoboken, N.J.)2024

Dexamethasone Inhibits the Growth of B-Lymphoma Cells by Downregulating DOT1L.

Yuting Wang, Nan Zhang, Weilong Shang, Huagang Peng, Zhen Hu, Yi Yang, Li Tan, Li Zhang, Fengtian He, Xiancai Rao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer reports (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yuting WangDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Nan ZhangDepartment of Hematology, People's Liberation Army the General Hospital of Western Theater Command, Chengdu, China.
Weilong ShangDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Huagang PengDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Zhen HuDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Yi YangDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Li TanDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.
Li ZhangDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, China.
Fengtian HeDepartment of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Army Medical University, Chongqing, China.
Xiancai RaoDepartment of Microbiology, College of Basic Medical Sciences, Key Laboratory of Microbial Engineering Under the Educational Committee in Chongqing, Army Medical University, Chongqing, China.ORCID 0000-0002-9905-760X

Funding

National Natural Science Foundation of China 81470325
6 · The paper itself

Abstract

backgroundDexamethasone (Dex), a synthetic glucocorticoid that acts by binding to the glucocorticoid receptor (GR), has been widely applied to treat leukemia and lymphoma; however, the precise mechanism underlying Dex action is still not well elucidated. DOT1L, a histone H3-lysine79 (H3K79) methyltransferase, has been linked to multiple cancer types, particularly mixed lineage leukemia (MLL) gene rearranged leukemia, but its contribution to lymphoma is yet to be delineated. Analysis from the TCGA database displayed that DOT1L was highly expressed in lymphoma and leukemia.

resultsWe initially demonstrated that DOT1L served as a new target gene controlled by GR, and the downregulation of DOT1L was critical for the killing of B-lymphoma cells by Dex. Further study revealed that Dex had no impact on the transcriptional activity of the DOT1L promoter, rather it reduced the mRNA level of DOT1L at the posttranscriptional level. In addition, knockdown of DOT1L remarkably inhibited the B-lymphoma cell growth.

conclusionsOverall, our findings indicated that DOT1L may serve as a potential drug target and a promising biomarker of Dex sensitivity when it comes to treating B lymphoma.

Indexed as

Cell ProliferationDexamethasoneHistone-Lysine N-MethyltransferaseLymphoma, B-CellMethyltransferasesReceptors, GlucocorticoidCell Line, TumorDown-RegulationGene Expression Regulation, NeoplasticHumansPromoter Regions, GeneticDexamethasoneDOT1L protein, humanHistone-Lysine N-MethyltransferaseMethyltransferasesReceptors, GlucocorticoiddexamethasoneDOT1Lgene regulationglucocorticoid receptor

Identifiers

PMID39307938
PMCPMC11417011

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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.