Evidence map›Paper›PMID 35999213›Full record

ArticleCell death discovery2022

Cancer associated fibroblasts secreted exosomal miR-1290 contributes to prostate cancer cell growth and metastasis via targeting GSK3β.

Shuo Wang, Peng Du, Yudong Cao, Jinchao Ma, Xiao Yang, Ziyi Yu, Yong Yang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  6. Hsa_circ_0030568 Promotes the Proliferation and Migration of Prostate Cancer CellsCombinatorial chemistry & high throughput screening · 2026
    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

7 authors at 1 institution in 2 countries.

Shuo Wang *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China.
Peng DuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China. dupeng9000@126.com.ORCID http://orcid.org/0000-0001-5843-4491
Yudong Cao *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China.
Jinchao Ma *Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China.
Xiao YangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China.
Ziyi YuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China.
Yong YangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Urological Department, Peking University Cancer Hospital & Institute, Bejing, 100142, PR China.
Ministry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts (CAFs) play crucial roles in mediating tumor growth and metastasis via transferring exosomes to neighboring cells, whereas the mechanisms by which CAFs regulate the tumorgenesis of prostate cancer (PC) remain largely unknown. In this study, CAFs and normal fibroblasts (NFs) were isolated from PC tissues and adjacent normal tissues, respectively. Exosomes (NFs-Exo and CAFs-Exo) were then isolated from the supernatant of NFs and CAFs. Next, the differentially expressed miRNAs (DEMs) between NFs-Exo and CAFs-Exo were identified using RNA-sequencing. Cell viability, migration and invasion were detected with CCK-8 and Transwell assays. Protein expression was measured with western blot. We found that CAFs-Exo remarkably enhanced PC cell migration, invasion, stemness, epithelial-mesenchymal transition (EMT) and metastasis. Significantly, miR-1290 level was upregulated in CAFs-Exo compared to NFs-Exo. In addition, CAFs could transfer exosomes to PC cells, resulting in a marked increase of miR-1290 level in cells. Moreover, exosomal miR-1290 could inhibit GSK3β/β-catenin signaling by binding with the downstream target GSK3β mRNA. Meanwhile, miR-1290 antagomir notably reversed the effects of CAFs-Exo on PC cells through activating GSK3β/β-catenin signaling. Collectively, exosomal miR-1290 from CAFs could promote PC cell growth and metastasis via inhibiting GSK3β/β-catenin signaling, suggesting that miR-1290 may serve as potential therapeutic target for the treatment of PC.

Identifiers

PMID35999213
PMCPMC9399109
OpenAlexW4292823553

What Socratic holds

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LicenceCC BY
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 Socratic graph.