Evidence map›Paper›PMID 39820521›Full record

ArticleOncology reports2025

Triple‑negative breast cancer cell‑derived piR‑31115 promotes the proliferation and migration of endothelial cells via METTL3‑mediated m6A modification of YAP1.

Shan-Mei Du, Na Li, Wen-Jing Xu, Kui Liu

Abstract read
In one paragraph

Article in Oncology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Clinical application and drug resistance mechanism of gemcitabine.Frontiers in cell and developmental biology · 2025
    Review
  4. Review
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

4 authors.

Shan-Mei DuSchool of Medicine, Zibo Vocational Institute, Zibo, Shandong 255300, P.R. China.
Na LiDepartment of Gastroenterology, Zhongda Hospital, Affiliated Hospital of Southeast University, Nanjing, Jiangsu 210009, P.R. China.
Wen-Jing XuDepartment of Hepatobiliary and Pancreatic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310009, P.R. China.
Kui LiuSchool of Medicine, Zibo Vocational Institute, Zibo, Shandong 255300, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Triple‑negative breast cancer (TNBC), a highly malignant breast cancer subtype with a pronounced metastatic propensity, forms the focus of the present investigation. MDA‑MB‑231, a prevalently utilized TNBC cell line in cancer research, was employed. In accordance with the tumour angiogenesis theory, cancer cells are capable of instigating angiogenesis and the formation of a novel vascular system within the tumour microenvironment, which subsequently sustains malignant proliferation and metastasis. Consequently, impeding the growth of tumour blood vessels holds substantial significance in suppressing TNBC metastasis. Piwi‑interacting RNAs (piRNAs), a category of endogenous non‑coding RNAs, have been demonstrated to modulate cancer progression. However, studies regarding the role of piRNAs in regulating angiogenesis within cancer cells are relatively scant. In the present study, via cell co‑culture experiments, it was revealed that piR‑31115 (a kind of piRNA) in MDA‑MB‑231 cells notably enhanced the recruitment of a human microvascular endothelial cell line (HMEC‑1). Moreover, the conditioned medium (CM, which was obtained from MDA‑MB‑231 cells via a specific culturing methodology and was employed for the subsequent treatment of HMEC‑1 cells to explore its impacts on the biological behaviors such as the proliferation and migration of HMEC‑1 cells) derived from MDA‑MB‑231 cells with upregulated piR‑31115 expression stimulated the proliferation and migration of HMEC‑1 cells. These findings suggest that piR‑31115 in MDA‑MB‑231 cells may play a pivotal role in modulating tumour angiogenesis. Further studies disclosed that the CM from MDA‑MB‑231 cells augmented the N6‑methyladenosine (m6A) RNA modification level via METTL3 in HMEC‑1 cells. Transcriptome sequencing revealed that METTL3 functions as an m6A writer protein for Yes‑associated protein 1 (YAP1), which exerts a positive influence on promoting the proliferation and migration of HMEC‑1 cells. Concurrently, the IGF2BP plays a crucial role in stabilizing YAP1 protein expression. Collectively, the present findings identified a signalling pathway through which MDA‑MB‑231 cells induce HMEC‑1 cell proliferation and migration by regulating m6A RNA methylation.

Indexed as

Adaptor Proteins, Signal TransducingEndothelial CellsMethyltransferasesRNA, Small InterferingTranscription FactorsTriple Negative Breast NeoplasmsAdenosineCell Line, TumorCell MovementCell ProliferationCoculture TechniquesFemaleGene Expression Regulation, NeoplasticHumansNeovascularization, PathologicTumor MicroenvironmentAdaptor Proteins, Signal TransducingAdenosineMethyltransferasesMETTL3 protein, humanN-methyladenosineRNA, Small InterferingTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsHMEC‑1IGFBP2METTL3Piwi‑interacting RNA‑31115triple‑negative breast cancerYes‑associated protein 1

Identifiers

PMID39820521
PMCPMC11755246

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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.