Evidence mapPaperPMID 36749775Full record

ArticlePloS one2023

Hsa-miR-22-3p inhibits liver cancer cell EMT and cell migration/ invasion by indirectly regulating SPRY2.

Shuaishuai Cui, Yuanyuan Chen, Yunfei Guo, Xing Wang, Dahu Chen

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2023. 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
5.5field-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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Poricoic Acid A attenuated TGF-β1-induced epithelial-mesenchymal transition in renal tubular epithelial cells through SPRY2/ERK signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Fecal miRNA Profiling of Yorkshire Terrier Enteropathy.International journal of molecular sciences · 2025
    Article
  9. Review
  10. The Role of microRNA-22 in Metabolism.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. 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

5 authors at 2 institutions in 1 country.

Shuaishuai CuiSchool of Life Sciences and Medicine, Shandong University of Technology, Zibo, China.
Yuanyuan ChenSchool of Life Sciences and Medicine, Shandong University of Technology, Zibo, China.
Yunfei GuoSchool of Life Sciences and Medicine, Shandong University of Technology, Zibo, China.
Xing WangSchool of Life Sciences, Jiangsu Normal University, Xuzhou, China.
Dahu ChenSchool of Life Sciences and Medicine, Shandong University of Technology, Zibo, China.ORCID 0000-0003-2470-2173
Shandong University of Technology · CNJiangsu Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The general mechanism for microRNAs to play biological function is through their inhibition on the expression of their target genes. In cancer, microRNAs may accelerate cell senescence, block angiogenesis, decrease energy supplies, repress tumor cell cycle and promote apoptosis to function as the tumor repressors. On the other hand, microRNAs can modulate tumor suppressor molecules to activate oncogene relevant signaling pathway to initiate tumorigenesis and promote tumor progression. By targeting different genes, miR-22 can function as either a tumor suppressor or a tumor promoter in different types of cancer. In liver cancer, miR-22 mainly functions as a tumor suppressor via its regulation on different genes. In this study, we demonstrated that miR-22 indirectly regulates SPRY2 by inhibiting CBL, an E3 ligase for SPRY2 that has been confirmed. As one of the modulators of the MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) signaling pathway, SPRY2 plays important roles in many developmental and physiological processes, and its deregulation has been reported in different types of cancer and shown to affect cancer development, progression, and metastasis. By inhibiting the expression of CBL, which stabilizes SPRY2, miR-22 indirectly upregulates SPRY2, thereby suppressing the epithelial-mesenchymal transition (EMT), cell migration, and invasion and decreasing the expression of liver cancer stem cell (CSC) marker genes. The inhibitory effects of miR-22 on EMT, cell migration, and invasion can be blocked by the knockdown of SPRY2 expression in miR-22 overexpressing cells. Additionally, we demonstrated that miR-22 expression inhibits the ERK signaling pathway and that this effect is due to its upregulation of SPRY2. Overall, our study revealed a novel miR-22-3p/CBL/SPRY2/ERK axis that plays an important role in EMT, cell migration, and invasion of liver cancer cells.

Indexed as

Liver NeoplasmsMicroRNAsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicroRNAsMIRN22 microRNA, humanSPRY2 protein, human

Identifiers

PMID36749775
PMCPMC9904474
OpenAlexW4319334429

What Socratic holds

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LicenceCC BY
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 Socratic graph.