Evidence map›Paper›PMID 22926525›Full record

ArticleOncogene2013

Histone methylase MLL1 has critical roles in tumor growth and angiogenesis and its knockdown suppresses tumor growth in vivo.

K I Ansari, S Kasiri, S S Mandal

Abstract read
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 77 citations in OpenAlex.

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  17. The role of KMT2 gene in human tumors.Histology and histopathology · 2022
    Review
  18. Article
  19. High Yap and Mll1 promote a persistent regenerative cell state induced by Notch signaling and loss of p53.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. 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

3 authors at 1 institution in 1 country.

K I AnsariDepartment of Chemistry and Biochemistry, The University of Texas at Arlington, Arlington, TX 76019, USA.
S Kasiri
S S Mandal
The University of Texas at Arlington · US

Funding

Endocrine Disruptors: Assessment of endocrine disruption activity, mechanism andR15ES019129 · NIEHS · UNIVERSITY OF TEXAS ARLINGTON · PI MANDAL, SUBHRANGSU S · 2010 to 2010
$445k
Redox-Active Ruthenium Complexes for Cancer TreatmentR15CA113747 · NCI · UNIVERSITY OF TEXAS ARLINGTON · PI MACDONNELL, FREDERICK M · 2006 to 2010
$436k
NCI NIH HHS 2R15 CA113747-02NCI NIH HHS R15 CA113747NIEHS NIH HHS 1R15 ES019129-01NIEHS NIH HHS R15 ES019129
6 · The paper itself

Abstract

Mixed lineage leukemias (MLLs) are human histone H3 lysine-4-specific methyl transferases that have critical roles in gene expression, epigenetics and cancer. Herein, we demonstrated that antisense-mediated knockdown of MLL1 induced cell-cycle arrest and apoptosis in cultured cells. Intriguingly, application of MLL1 antisense specifically knocked down MLL1 in vivo and suppressed the growth of xenografted cervical tumor implanted in nude mouse. MLL1 knockdown downregulated various growth and angiogenic factors, such as HIF1α, VEGF and CD31, in tumor tissue affecting tumor growth. MLL1 is overexpressed along the line of vascular network and localized adjacent to endothelial cell layer expressing CD31, indicating potential roles of MLL1 in vasculogenesis. MLL1 is also overexpressed in the hypoxic regions along with HIF1α. Overall, our studies demonstrated that MLL1 is a key factor in hypoxia signaling, vasculogenesis and tumor growth, and its depletion suppresses tumor growth in vivo, indicating its potential in novel cancer therapy.

Indexed as

Gene Knockdown TechniquesAnimalsApoptosisCell CycleCell HypoxiaCell Line, TumorCell ProliferationCell SurvivalCell Transformation, NeoplasticFemaleHistone-Lysine N-MethyltransferaseHumansMiceMyeloid-Lymphoid Leukemia ProteinNeovascularization, PathologicSignal TransductionHistone-Lysine N-MethyltransferaseKMT2A protein, humanMyeloid-Lymphoid Leukemia Protein

Identifiers

PMID22926525
PMCPMC3511651
OpenAlexW2075867957

What OpenQuestion holds

Textmetadata
LicenceTDM
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.