Evidence map›Paper›PMID 35520918›Full record

ArticleRSC advances2019

LncRNA HOTAIRM1 is involved in the progression of acute myeloid leukemia through targeting miR-148b.

Ning Hu, Li Chen, Qianyu Li, Hongmian Zhao

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Article in RSC advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

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4 · The record

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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

4 authors.

Ning HuDepartment of Hematology, Huaihe Hospital of Henan University No. 115 Ximen Street Kaifeng 475000 Henan China zhhm6039@163.com.
Li ChenDepartment of Hematology, Huaihe Hospital of Henan University No. 115 Ximen Street Kaifeng 475000 Henan China zhhm6039@163.com.
Qianyu LiDepartment of Hematology, Huaihe Hospital of Henan University No. 115 Ximen Street Kaifeng 475000 Henan China zhhm6039@163.com.
Hongmian ZhaoDepartment of Hematology, Huaihe Hospital of Henan University No. 115 Ximen Street Kaifeng 475000 Henan China zhhm6039@163.com.ORCID https://orcid.org/0000-0001-9640-0305

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LncRNAs have been shown to be involved in the biological and pathological processes of acute myeloid leukemia (AML). Hox antisense intergenic RNA myeloid 1 (HOTAIRM1) was reported to be highly expressed in AML. However, the detailed role and molecular mechanism of HOTAIRM1 in AML pathogenesis remain undefined. In the present study, HOTAIRM1 and miR-148b expressions in AML patients and healthy controls were detected by qRT-PCR. Cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry assays, respectively. The regulatory interaction between HOTAIRM1 and miR-148b was explored by bioinformatics analysis using starBase v3.0 software and The Cancer Genome Atlas (TCGA) AML dataset. We found that the miR-148/miR-152 family members including miR-148a, miR-148b, and miR-152 were predicted to be potential targets of HOTAIRM1. HOTAIRM1 expression was negatively correlated with miR-148b expression but had no correlation with miR-148a/miR-152 expressions in AML samples from the TCGA dataset. HOTAIRM1 expression was higher while miR-148b expression was lower in AML patients than in healthy controls. A negative correlation between HOTAIRM1 and miR-148b in AML patients was observed. HOTAIRM1 silencing and miR-148b overexpression both suppressed cell proliferation and induced apoptosis in AML cells. miR-148b was identified as a target of HOTAIRM1 in AML cells. Moreover, HOTAIRM1 knockdown inhibited proliferation and induced apoptosis in AML cells by negatively regulating miR-148b. In summary, HOTAIRM1 was involved in the progression of AML through targeting miR-148b, shedding light on the biological function and molecular mechanism of HOTAIRM1 in AML.

Identifiers

PMID35520918
PMCPMC9062379

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