Evidence map›Paper›PMID 32945512›Full record

ArticleOncology reports2020

MicroRNA‑137 exerts protective effects on hypoxia‑induced cell injury by inhibiting autophagy/mitophagy and maintaining mitochondrial function in breast cancer stem‑like cells.

Qiongying Hu, Yun Yuan, Yeke Wu, Yongliang Huang, Ziyi Zhao, Chong Xiao

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 21% of its field
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

22 citing papers in PubMed, 28 citations in OpenAlex.

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  18. The multi-faced role of FUNDC1 in mitochondrial events and human diseases.Frontiers in cell and developmental biology · 2022
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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 at 2 institutions in 1 country.

Qiongying Hu *Department of Laboratory Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Yun Yuan *College of Medical Technology, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Yeke WuDepartment of Stomatology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Yongliang HuangDepartment of Pharmacy, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Ziyi ZhaoDepartment of Central Laboratory, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Chong XiaoTeaching and Research Office of Oncology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 610072, P.R. China.
Chengdu University of Traditional Chinese Medicine · CNStomatology Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer stem‑like cells (BCSCs) have been identified and proven to play critical roles in tumorigenesis and progression. Hypoxia is a common pathologic feature of breast cancer and potentially, at least in part, regulates the initiation, progression, and recurrence of breast cancer. However, less is known about how hypoxia regulates BCSCs. As several well‑known microRNAs respond to hypoxia, we aimed to determine how hypoxia regulates the physiological processes of BCSCs by regulating the corresponding microRNAs. As expected, microRNA‑137 (miRNA‑137 or miR‑137) was downregulated upon hypoxic exposure, indicating that it may play critical roles in BCSCs. Introduction of miR‑137 mimics promoted cell cycle entry and inhibited hypoxia‑induced cell apoptosis as determined by cell cycle assay and apoptosis assay. By detecting mitochondrial reactive oxygen species (ROS), it was found that miR‑137 inhibited ROS accumulation induced by hypoxic exposure and thus suppressed cell apoptosis. Introduction of miR‑137 mimics under hypoxia inhibited mitophagy/autophagy by targeting FUN14 domain containing 1 (Fundc1) and thus promoted mitochondrial functions, including mitochondrial mass, ATP synthesis and mitochondrial transcriptional activity, which was similar to the effects of Fundc1 knockdown by specific siRNA. Based on these observations, we hypothesized that the survival of BCSCs under hypoxia was mediated by miR‑137 by regulating mitochondrial dysfunction. We demonstrated here that the introduction of exogenous miR‑137 promoted mitochondrial function, indicating that it may be a potential therapeutic target in BCSCs.

Indexed as

ApoptosisAutophagyBreast NeoplasmsFemaleHumansMembrane ProteinsMicroRNAsMitochondriaMitochondrial ProteinsMitophagyNeoplastic Stem CellsReactive Oxygen SpeciesTumor HypoxiaFUNDC1 protein, humanMembrane ProteinsMicroRNAsMIRN137 microRNA, humanMitochondrial ProteinsReactive Oxygen Speciesbreast cancer stem‑like cellshypoxiamiR‑137mitochondrial dysfunctionreactive oxygen species

Identifiers

PMID32945512
PMCPMC7448477
OpenAlexW3047189325

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.