Evidence map›Paper›PMID 38956502›Full record

ArticleCellular & molecular biology letters2024

LncRNA TRPM2-AS promotes endometrial carcinoma progression and angiogenesis via targeting miR-497-5p/SPP1 axis.

Hanbo Ma, Fengyun Weng, Xiaowen Tong, Huaifang Li, Yinan Yao, Jiangjing Yuan

Abstract read
In one paragraph

Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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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

6 authors.

Hanbo MaDepartment of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China.
Fengyun WengDepartment of Obstetrics and Gynecology, Shangyu People's Hospital of Shaoxing, Zhejiang, 312300, China.
Xiaowen TongDepartment of Obstetrics and Gynecology, Tongji Hospital of Tongji University, Tongji University School of Medicine, Shanghai, 200065, China.
Huaifang LiDepartment of Obstetrics and Gynecology, Tongji Hospital of Tongji University, Tongji University School of Medicine, Shanghai, 200065, China. huaifangli@126.com.
Yinan YaoDepartment of Obstetrics and Gynecology, Tongji Hospital of Tongji University, Tongji University School of Medicine, Shanghai, 200065, China. yinanyao@126.com.
Jiangjing YuanDepartment of Obstetrics and Gynecology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China. drtracy80@sina.com.

Funding

National Natural Science Foundation of China 81873827Shanghai Science and Technology Commission 21Y11906600
6 · The paper itself

Abstract

backgroundAnti-angiogenic therapy has become one of the effective treatment methods for tumors. Long noncoding RNAs (lncRNAs) are emerging as important regulators of tumorigenesis and angiogenesis in EC. However, the underlying mechanisms of lncRNA TRPM2-AS in EC are still not clear.

methodsWe screened the differently expressed lncRNAs that were highly associated with poor prognosis and angiogenesis of EC by bioinformatics analysis, and constructed a ceRNA network based on the prognostic lncRNAs. The subcellular localization of TRPM2-AS was determined by fluorescence in situ hybridization (FISH) and nuclear cytoplasmic fractionation assay. CCK-8, EdU, transwell, western blot, qRT-PCR and endothelial tube formation assay were used to evaluate the effects of TRPM2-AS on the proliferation, invasion, migration of EC cells and angiogenesis. The targeted microRNA (miRNA) of TRPM2-AS was predicted by bioinformatic methods. The interaction between TRPM2-AS and miR497-5p, miR497-5p and SPP1 were analyzed by RNA immunoprecipitation and dual-luciferase reporter assay. A subcutaneous tumor model was used to explore TRPM2-AS's function in vivo. CIBERSORT was used to analyze the correlation between TRPM2-AS and immune cell immersion in EC.

resultsWe found that the expression of TRPM2-AS and SPP1 was aberrantly upregulated, while miR-497-5p expression was significantly downregulated in EC tissues and cells. TRPM2-AS was closely correlated with the angiogenesis and poor prognosis in EC patients. Mechanistically, TRPM2-AS could sponge miR-497-5p to release SPP1, thus promoting the proliferation, invasion and migration of EC cells and angiogenesis of HUVECs. Knockdown of TRPM2-AS in xenograft mouse model inhibited tumor proliferation and angiogenesis in vivo. In addition, TRPM2-AS plays a vital role in regulating the tumor immune microenvironment of EC, overexpression of TRPM2-AS in EC cells stimulated the polarization of M2 macrophages and angiogenesis through secreting SPP1 enriched exosomes.

conclusionThe depletion of TRPM2-AS inhibits the oncogenicity of EC by targeting the miR-497-5p/SPP1 axis. This study offers a better understanding of TRPM2-AS's role in regulating angiogenesis and provides a novel target for EC treatment.

Indexed as

Cell MovementCell ProliferationEndometrial NeoplasmsGene Expression Regulation, NeoplasticMicroRNAsNeovascularization, PathologicRNA, Long NoncodingAngiogenesisAnimalsCell Line, TumorDisease ProgressionFemaleHumansMiceMice, Inbred BALB CMice, NudeMicroRNAsMIRN497 microRNA, humanRNA, Long NoncodingTRPM Cation ChannelsAngiogenesisEndometrial carcinomaLncRNA TRPM2-ASMiR-497-5pSPP1

Identifiers

PMID38956502
PMCPMC11218065

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.