Evidence map›Paper›PMID 33154575›Full record

ArticleCancer gene therapy2021

Elevating microRNA-1-3p shuttled by cancer-associated fibroblasts-derived extracellular vesicles suppresses breast cancer progression and metastasis by inhibiting GLIS1.

Shuang Tao, Hong Li, Xiuzhen Ma, Yunfei Ma, Jiale He, Yali Gao, Jinping Li

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2021. 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
–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

29 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

7 authors.

Shuang Tao *Department of Breast Surgery, Changzhou No. 7 People's Hospital, 213000, Changzhou, P. R. China.
Hong Li *Department of Surgical Oncology, General Hospital of Ningxia Medical University, 750004, Yinchuan, P. R. China.
Xiuzhen Ma *Department of Surgical Oncology, General Hospital of Ningxia Medical University, 750004, Yinchuan, P. R. China.
Yunfei MaNingxia Medical University, 750004, Yinchuan, P. R. China.
Jiale HeNingxia Medical University, 750004, Yinchuan, P. R. China.
Yali GaoNingxia Medical University, 750004, Yinchuan, P. R. China.
Jinping LiDepartment of Surgical Oncology, General Hospital of Ningxia Medical University, 750004, Yinchuan, P. R. China. lijinping@nxmu.edu.cn.ORCID http://orcid.org/0000-0001-7706-0587

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) play supporting roles in tumor progression by releasing microvesicles that transmit oncogenic cargoes. Indeed, extracellular vesicles (EVs) have emerged as important vehicles to deliver proteins, messenger RNAs (mRNAs), and microRNAs (miRs) between cells. In this study, we aimed to outline the role and function of CAFs-derived EVs carrying miR-1-3p in breast cancer. We first experimentally determined downregulated miR-1-3p in breast cancer tissues. EVs were isolated from CAFs extracted from breast cancer tissues, which showed downregulated miR-1-3p expression relative to EVs derived from normal fibroblasts (NFs). In a co-culture system, miR-1-3p cargo was transported into breast cancer cells via CAF-derived EVs. In gain-of-function experiments, the elevation of miR-1-3p in breast cancer cells inhibited cell viability, invasion, migration, and epithelial-to-mesenchymal transition, and suppressed tumor formation and metastasis. Furthermore, EVs derived from CAFs transfected with miR-1-3p mimic were more effective in transferring miR-1-3p to suppress cancer progression and metastasis. Krüppel-like zinc-finger protein Gli-similar 1 (GLIS1) was predicted to be a putative target of miR-1-3p, which was subsequently confirmed by dual-luciferase reporter assay. We then demonstrated that overexpression of GLIS1 neutralized the effects of miR-1-3 on the development of breast cancer in vitro. These findings shed light on the underlying mechanism by which CAFs-derived EVs carrying miR-1-3p mediate the progression and metastasis of breast cancer, and highlight the potential of miR-1-3p shuttled by CAFs-derived EVs serving as a therapeutic target for breast cancer.

Indexed as

Breast NeoplasmsCancer-Associated FibroblastsCell ProliferationCell SurvivalDisease ProgressionDNA-Binding ProteinsEpithelial-Mesenchymal TransitionExtracellular VesiclesFemaleGain of Function MutationHumansMicroRNAsNeoplasm InvasivenessNeoplasm MetastasisTranscription FactorsDNA-Binding ProteinsGLIS1 protein, humanMicroRNAsMIRN1 microRNA, humanTranscription Factors

Identifiers

PMID33154575

What OpenQuestion holds

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Registered trials

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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.