Evidence map›Paper›PMID 32174262›Full record

ArticleTechnology in cancer research & treatment

miR-331-3p Suppresses Cell Proliferation in TNBC Cells by Downregulating NRP2.

Mingchuan Zhao, Mengmeng Zhang, Zhonghua Tao, Jun Cao, Leiping Wang, Xichun Hu

Abstract read
In one paragraph

Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

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  9. LncRNA HOTAIR enhances RCC2 to accelerate cervical cancer progression by sponging miR-331-3p.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  10. Review
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  12. Neuropilin (NRPs) Related Pathological Conditions and Their Modulators.International journal of molecular sciences · 2022
    Review
  13. Article
  14. Article
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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.

Mingchuan ZhaoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University School of Medicine, Shanghai, People's Republic of China.
Mengmeng ZhangNational Center for Drug Screening, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, People's Republic of China.
Zhonghua TaoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University School of Medicine, Shanghai, People's Republic of China.
Jun CaoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University School of Medicine, Shanghai, People's Republic of China.
Leiping WangDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University School of Medicine, Shanghai, People's Republic of China.
Xichun HuDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University School of Medicine, Shanghai, People's Republic of China.ORCID 0000-0002-3488-6394

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTriple-negative breast cancer is characterized by fast progression with high possible for metastasis and poor survival. Dysfunction of microRNAs plays an important role in the initiation and progression of cancer. Our previous microRNA-seq data indicated the downregulation of miR-331-3p in triple-negative breast cancer tissues compared with that of the noncancer tissues. However, the function of miR-331-3p in triple-negative breast cancer remains largely unknown. Herein, the involvement of miR-331-3p in triple-negative breast cancer was investigated and the therapeutic potential of miR-331-3p was also explored.

methodsReal-time quantitative polymerase chain reaction was performed to detect the expression of miR-331-3p in triple-negative breast cancer tissues and cell lines. The cell proliferation was determined by the cell counting kit-8 assay. Apoptosis of triple-negative breast cancer cells was examined by annexin V/propidium iodide staining. miRDB database was used to predict the potential targets of miR-331-3p. Western blot was performed to examine the expression of the target protein.

resultsmiR-331-3p was significantly downregulated in triple-negative breast cancer tissues and cell line. Lower miR-331-3p expression was significantly correlated with the tumor size, TNM stage, and lymph node metastasis of patients with triple-negative breast cancer. Functional experiments showed that the overexpression of miR-331-3p inhibited the proliferation and increased apoptosis of triple-negative breast cancer cells. Neuropilin-2 was identified as a target of miR-331-3p, which harbored binding site of miR-331-3p in its 3'-untranslated region. Overexpression of miR-331-3p decreased the messenger RNA and protein levels of neuropilin-2 in triple-negative breast cancer cells. Restoration of neuropilin-2 partially reversed the inhibitory effects of miR-331-3p on the proliferation of triple-negative breast cancer cells.

conclusionsOur results demonstrated the novel function of miR-331-3p/neuropilin-2 signaling in regulating the malignant behaviors of triple-negative breast cancer cells, which suggested miR-331-3p as a potential target for the treatment of triple-negative breast cancer.

Indexed as

ApoptosisCell ProliferationGene Expression Regulation, NeoplasticCell Line, TumorCell MovementDisease ProgressionFemaleHumansMicroRNAsMiddle AgedNeuropilin-2Signal TransductionTriple Negative Breast NeoplasmsMicroRNAsMIRN331 microRNA, humanNeuropilin-2neuropilin-2, humanmiR-331-3pNRP2TNBC

Identifiers

PMID32174262
PMCPMC7076578

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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.