Evidence map›Paper›PMID 36182945›Full record

ArticleBiological research2022

Melanoma stem cells promote metastasis via exosomal miR-1268a inactivation of autophagy.

Xiaoshuang Li, Doudou Liu, Hao Chen, Bin Zeng, Qiting Zhao, Yuhan Zhang, Yuting Chen, Jianyu Wang, H Rosie Xing

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  4. Exosomes, autophagy, and cancer: A complex triad.International journal of cancer · 2025
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  10. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
    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

9 authors at 1 institution in 1 country.

Xiaoshuang LiState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China.
Doudou Liu *State Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China.
Hao ChenState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China.
Bin ZengInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Qiting ZhaoInstitute of Life Sciences, Chongqing Medical University, Chongqing, China.
Yuhan Zhang *State Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China.
Yuting ChenState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China.
Jianyu WangInstitute of Life Sciences, Chongqing Medical University, Chongqing, China. 102758@cqmu.edu.cn.
H Rosie XingState Key Laboratory of Ultrasound in Medicine and Engineering, College of Biomedical Engineering, Chongqing Medical University, Chongqing, 400016, China. 102643@cqmu.edu.cn.
Chongqing Medical University · CN

Funding

National Natural Science Foundation of China 82073277National Natural Science Foundation of China 82173247
6 · The paper itself

Abstract

backgroundMetastatic melanoma has a high mortality rate and poor survival. This is associated with efficient metastatic colonization, but the underlying mechanisms remain elusive. Communication between cancer stem cells (CSCs) and cancer cells plays an important role in metastatic dissemination. Whether cancer stem cells can alter the metastatic properties of non-CSC cells; and whether exosomal crosstalk can mediate such interaction, have not been demonstrated in melanoma prior to this report.

resultsThe results revealed that exosomes secreted by highly metastatic melanoma CSCs (OL-SCs) promoted the invasiveness of the low metastatic melanoma cells (OL) and accelerated metastatic progression. miR-1268a was up-regulated in cells and exosomes of OL-SCs. Moreover, OL-SCs-derived exosomal miR-1268a, upon taking up by OL cells, promoted the metastatic colonization ability of OL cells in vitro and in vivo. In addition, the pro-metastatic activity of exosomal miR-1268a is achieved through inhibition of autophagy.

conclusionOur study demonstrates that OL cells can acquire the "metastatic ability" from OL-SCs cells. OL-SCs cells achieves this goal by utilizing its exosomes to deliver functional miRNAs, such as miR-1268a, to the targeted OL cells which in turn augments metastatic colonization by inactivating the autophagy pathway in OL cells.

Indexed as

ExosomesMelanomaMicroRNAsAutophagyCell Line, TumorHumansNeoplasm MetastasisStem CellsMicroRNAsAutophagyExosomesMelanoma stem cellsMetastasismiR-1268a

Identifiers

PMID36182945
PMCPMC9526915
OpenAlexW4298325558

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.