Evidence map›Paper›PMID 28745315›Full record

ArticleOncogene2017

miR-302/367/LATS2/YAP pathway is essential for prostate tumor-propagating cells and promotes the development of castration resistance.

Y Guo, J Cui, Z Ji, C Cheng, K Zhang, C Zhang, M Chu, Q Zhao, Z Yu, Y Zhang and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
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  14. Cancer Stem Cells: An Ever-Hiding Foe.Experientia supplementum (2012) · 2022
    Article
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  16. Article
  17. Article
  18. Review
  19. Long non‑coding RNAInternational journal of molecular medicine · 2021
    Article
  20. MiR-92 overexpression suppresses immune cell function in ovarian cancer via LATS2/YAP1/PD-L1 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
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

13 authors at 2 institutions in 1 country.

Y GuoState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
J CuiState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Z JiSchool of Biomedical Engineering & Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-0562-2477
C ChengSchool of Biomedical Engineering & Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
K ZhangSchool of Biomedical Engineering & Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
C ZhangState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
M ChuState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Q ZhaoResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Z YuResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0003-4196-9662
Y ZhangResearch Center for Translational Medicine, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Y-X FangState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
W-Q GaoState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
H H ZhuState Key Laboratory of Oncogenes and Related Genes, Ren ji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Jiao Tong University · CNShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical intervention for patients with advanced prostate cancer (PCa) remains challenging due to the inevitable recurrence of castration-resistant prostate cancer (CRPC) after androgen deprivation therapy (ADT). Cancer stem cells (CSCs) with serial tumor-propagating capacity are considered to be the driving force for PCa progression and recurrence. In this study, we report that the miR-302/367 cluster, a previously identified potent pluripotency regulator, is upregulated in prostate tumors. Specifically, the forced expression of the miR-302/367 cluster accelerates the in vitro and in vivo growth of PCa cells and their resistance to androgen ablation, whereas the knockdown of the miR-302/367 cluster using anti-sense RNA suppresses the incidence of formation, growth rate and endpoint weight of PCa cell tumors. Mechanistically, we find that LATS2, a key component of the tumor-suppressive Hippo signaling pathway, acts as a direct target of the miR-302/367 cluster in PCa cells. The downregulation of LATS2 by the miR-302/367 cluster reduces the phosphorylation and enhances the nuclear translocation of the YAP oncoprotein. Conversely, the restoration of LATS2 expression abrogates the tumor-promoting effects of forced miR-302/367 cluster expression. Collectively, the potent pluripotency regulator-triggered miR-302/367/LATS2/YAP pathway is essential for prostate tumor-propagating cells and promotes castration resistance. Thus, targeting this signaling axis may represent a promising therapeutic strategy for CRPC.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell Line, TumorCell ProliferationHEK293 CellsHumansMaleMiceMice, Inbred BALB CMicroRNAsNeoplasm Recurrence, LocalNuclear ProteinsPhosphoproteinsProstatic Neoplasms, Castration-ResistantProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingCell Cycle ProteinsLATS2 protein, humanLATS2 protein, mouseMicroRNAsMIRN302 microRNA, mouseMIRN367 microRNA, humanMIRN367 microRNA, mouseNuclear ProteinsPhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsTumor Suppressor ProteinsYap1 protein, mouseYAP-Signaling ProteinsYY1AP1 protein, human

Identifiers

PMID28745315
OpenAlexW2737749063

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.