Evidence map›Paper›PMID 42047981›Full record

ArticleInternational urology and nephrology2026

Tumor-derived extracellular vesicles exert promotional effects on metastasis in renal cell carcinoma through the delivery of microRNA-671-5p.

Xiaohui Huang, Tianli Shi, Jinbiao Zhou, Fusheng Peng

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Article in International urology and nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper 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.

Xiaohui HuangFifth School of Clinical Medicine of Zhejiang, Chinese Medical University, Huzhou, 313003, Zhejiang, China.
Tianli ShiFifth School of Clinical Medicine of Zhejiang, Chinese Medical University, Huzhou, 313003, Zhejiang, China.
Jinbiao ZhouFifth School of Clinical Medicine of Zhejiang, Chinese Medical University, Huzhou, 313003, Zhejiang, China.
Fusheng PengFifth School of Clinical Medicine of Zhejiang, Chinese Medical University, Huzhou, 313003, Zhejiang, China. haal_19@163.com.

Funding

Huzhou Science and Technology Bureau 2021GY07
6 · The paper itself

Abstract

purposeTumor-derived extracellular vesicles (EVs) can deliver microRNAs (miRNAs) to promote tumor development. Herein, this study explored whether tumor-derived EVs carrying miR-671-5p facilitated renal cell carcinoma (RCC) cell growth.

methodsmiR-671-5p expression in RCC cells and the collected EVs was assessed. After gain- and loss-of-function assays and EV co-culture, cell viability, invasion and migration, and apoptosis were measured. RNA pull-down and dual-luciferase reporter assays were used to analyze the binding between miR-671-5p and inhibitor of growth 5 (ING5). The function of EVs in RCC metastasis in vivo was evaluated through tumor transplantation in nude mice.

resultsmiR-671-5p was up-regulated in RCC cells and EVs from ACHN cells. miR-671-5p down-regulation inhibited RCC cell proliferation, invasion, and migration but accelerated cell apoptosis. EVs derived from ACHN cells carried miR-671-5p into RCC cells. RCC cell invasion, migration, and proliferation were diminished but cell apoptosis was elevated after co-culture with EVs carrying inhibitors-miR-671-5p. Mechanistically, ING5 was a target of miR-671-5p. ING5 silencing abrogated the effects of EVs carrying inhibitors-miR-671-5p on RCC cells. EVs accelerated tumor growth, increased tumor volume, and elevated Ki-67-positive cells in mice, accompanied by increased miR-671-5p expression and decreased ING5 expression, whereas EVs carrying inhibitors-miR-671-5p contributed to opposite results.

conclusionTumor-derived EVs carrying miR-671-5p target ING5 to promote RCC cell growth.

Indexed as

Carcinoma, Renal CellExtracellular VesiclesKidney NeoplasmsMicroRNAsAnimalsApoptosisCell Line, TumorCell MovementCell ProliferationHumansMiceMice, NudeNeoplasm InvasivenessNeoplasm MetastasisTranscription FactorsTumor Suppressor ProteinsING5 protein, humanMicroRNAsTranscription FactorsTumor Suppressor ProteinsExtracellular vesiclesInhibitor of growth 5InvasionmicroRNA-671-5pMigrationProliferationRenal cell carcinoma

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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.