Evidence map›Paper›PMID 32108166›Full record

ArticleOncogene2020

MiR-629-5p promotes the invasion of lung adenocarcinoma via increasing both tumor cell invasion and endothelial cell permeability.

Yu Li, Huibiao Zhang, Lei Fan, Jiahui Mou, Yue Yin, Chao Peng, Yuxiang Chen, Henglei Lu, Liting Zhao, Zhouteng Tao and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  19. Noncoding RNAs in tumor metastasis: molecular and clinical perspectives.Cellular and molecular life sciences : CMLS · 2021
    Review
  20. Non-coding RNA in cancer.Essays in biochemistry · 2021
    Review
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

15 authors at 4 institutions in 1 country.

Yu Li *Center for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Huibiao Zhang *Department of Thoracic Surgery, Huadong Hospital, Fudan University, 200040, Shanghai, China.
Lei FanCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Jiahui MouCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Yue YinNational Facility for Protein Science in Shanghai, Zhangjiang Lab, 201210, Shanghai, China.
Chao PengShanghai Science Research Center, Chinese Academy of Sciences, 201204, Shanghai, China.
Yuxiang ChenCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Henglei LuCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Liting ZhaoDepartment of Nursing, Huadong Hospital, Fudan University, 200040, Shanghai, China.
Zhouteng TaoCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Jing ChenCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Yizheng WangThe Brain Science Center, Beijing Institute of Basic Medical Sciences, 100730, Beijing, China.
Xinming QiCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China.
Ruimin HuangUniversity of Chinese Academy of Sciences, 100049, Beijing, China. rmhuang@simm.ac.cn.ORCID http://orcid.org/0000-0001-9369-0263
Jin RenCenter for Drug Safety Evaluation and Research, State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, 201203, Shanghai, China. jren@cdser.simm.ac.cn.
Chinese Academy of Sciences · CNFudan University · CNShanghai Institute of Materia Medica · CNChinese Institute for Brain Research · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor invasion underlies further metastasis, the leading cause for cancer-related deaths. Deregulation of microRNAs has been identified associated with the malignant behavior of various cancers, including lung adenocarcinoma (LUAD), the major subtype of lung cancer. Here, we showed the significantly positive correlation between miR-629-5p level and tumor invasion in LUAD specimens (n = 49). In a human LUAD metastasis mouse model, H1650 cells (high level of miR-629-5p) were more aggressive than A549 cells (low level of miR-629-5p) in vivo, including higher incidence of vascular invasion and pulmonary colonization. Ectopic expression of miR-629-5p in A549 cells also increased their invasive capability. Then we identified that miR-629-5p promotes LUAD invasion in a mode of dual regulation via tumor cells invasion and endothelial cells permeability, respectively. In tumor cells, miR-629-5p enhanced motility and invasiveness of tumor cells by directly targeting PPWD1 (a cyclophilin), which clinically related to tumor invasion in LUAD specimens. Restoring PPWD1 protein significantly attenuated the invasion-promoting effects of miR-629-5p. Besides, exosomal-miR-629-5p secreted from tumor cells could be transferred to endothelial cells and increased endothelial monolayers permeability by suppressing CELSR1 (a nonclassic-type cadherin), which had a low level in the endothelial cells of invasive LUAD specimens. Activating the expression of CELSR1 in endothelial cells markedly blocked the effect of miR-629-5p. Our study suggests the dual roles of miR-629-5p in tumor cells and endothelial cells for LUAD invasion, implying a therapeutic option to targeting miR-629-5p using the "one stone, two birds" strategy in LUAD.

Indexed as

A549 CellsAdenocarcinoma of LungBiomarkers, TumorCadherinsEndothelial CellsHEK293 CellsHumansLung NeoplasmsMicroRNAsNeoplasm InvasivenessNeoplasm ProteinsPermeabilityRNA, NeoplasmBiomarkers, TumorCadherinsCELSR1 cadherin, humanMicroRNAsMIRN629 microRNA, humanNeoplasm ProteinsRNA, Neoplasm

Identifiers

PMID32108166
OpenAlexW3008758622

What OpenQuestion holds

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Read underepoch 390

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.