Evidence map›Paper›PMID 35292358›Full record

ArticleCellular signalling2022

LncRNA HOTAIR sponges miR-301a-3p to promote glioblastoma proliferation and invasion through upregulating FOSL1.

Shanchun Guo, Pendelton King, Emily Liang, Alyssa A Guo, Mingli Liu

Open access · hybridAbstract read
In one paragraph

Article in Cellular signalling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 35 citations in OpenAlex.

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  16. Interaction of NF-κB and FOSL1 drives glioma stemness.Cellular and molecular life sciences : CMLS · 2024
    Article
  17. Review
  18. Review
  19. Review
  20. The multifaceted functions of long non-coding RNAExpert reviews in molecular medicine · 2024
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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

5 authors at 3 institutions in 1 country.

Shanchun GuoDepartment of Chemistry, Xavier University, 1 Drexel Dr, New Orleans, LA, United States of America.
Pendelton KingDepartment of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA, United States of America.
Emily LiangDepartment of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA, United States of America.
Alyssa A GuoUniversity of South Carolina SOM Greenville, Greenville, SC, United States of America.
Mingli LiuDepartment of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA, United States of America. Electronic address: mliu@msm.edu.
Morehouse School of Medicine · USUniversity of South Carolina · USXavier University · US

Funding

TRPM7 induces tumorigenesis and stemness through Notch activation in gliomaSC1GM144021 · NIGMS · MOREHOUSE SCHOOL OF MEDICINE · PI LIU, MINGLI · 2022 to 2025
$1.4M
The Role of TRPM7 in Progression of Malignant GliomaSC3GM121230 · NIGMS · MOREHOUSE SCHOOL OF MEDICINE · PI LIU, MINGLI · 2018 to 2021
$426k
NIGMS NIH HHS SC1 GM144021NIGMS NIH HHS SC3 GM121230
6 · The paper itself

Abstract

Glioblastoma, one of the most fatal brain tumors, is associated with a dismal prognosis and an extremely short overall survival. We previously reported that the overexpressed transient receptor potential channel TRPM7 is an essential glioblastoma regulator. Accumulating evidence suggests that long noncoding RNAs (lncRNAs) play an important role in glioma's initiation and progression. However, the function of lncRNA, HOX transcript antisense intergenic RNA (HOTAIR) mediated by TRPM7 in glioma remains unclear. In this study, HOTAIR expression was found to be positively regulated by TRPM7, significantly upregulated in glioma tissues, and is a poor prognosis factor for glioma patients. Moreover, reduced HOTAIR expression impeded the proliferation and invasion of glioma cells. Mechanistically, HOTAIR directly interacted with miR-301a-3p, and downregulation of miR-301a-3p efficiently reversed FOSL1 suppression induced by siRNA HOTAIR, which implied that HOTAIR positively regulated FOSL1 level through sponging miR-301a-3p and played an oncogenic role in glioma progression. In contrast to HOTAIR's role, miR-301a-3p alone served as a tumor suppressor to decrease glioma cell viability and migration/invasion. In agreement with HOTAIR's role, FOSL1 functioned as a tumorigenic gene in glioma pathogenesis, which was highly expressed in glioma tissues, and was shown to be an unfavorable prognostic factor for glioma patients. Mechanically, FOSL1 inhibition by siRNA FOSL1 efficiently rescued the oncogenic-like phenotypes caused by the miR-301a-3p inhibitor in glioma pathogenesis. SIGNIFICANCE: Our study elucidated the role of TRPM7-mediated HOTAIR as a miRNA sponge to target downstream FOSL1 oncogene and therefore consequently contribute to gliomagenesis, which shed new light on TRPM7/lncRNA-directed diagnostic and therapeutic approach in glioma.

Indexed as

GlioblastomaGliomaMicroRNAsTRPM Cation ChannelsCarcinogenesisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansProtein Serine-Threonine KinasesRNA, Long NoncodingRNA, Small InterferingHOTAIR long untranslated RNA, humanMicroRNAsProtein Serine-Threonine KinasesRNA, Long NoncodingRNA, Small InterferingTRPM7 protein, humanTRPM Cation ChannelsFOSL1GliomaHOTAIRmiR-301a-3pTRPM7

Identifiers

PMID35292358
PMCPMC9058208
OpenAlexW4220833225

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.