Evidence map›Paper›PMID 30988277›Full record

ArticleCell death & disease2019

MicroRNA-196a/-196b regulate the progression of hepatocellular carcinoma through modulating the JAK/STAT pathway via targeting SOCS2.

Weihua Ren, Shuangting Wu, Yabin Wu, Tan Liu, Xingpeng Zhao, Yawei Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

45 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. STAT1 suppresses the transcriptional activity of TRIM21 in gastric cancer.Journal of cancer research and clinical oncology · 2023
    Article
  18. Article
  19. Review
  20. 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

6 authors at 1 institution in 1 country.

Weihua RenMedical Diagnostic Centre, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Shuangting WuDepartment of Anesthesiology, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Yabin WuMedical Diagnostic Centre, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Tan LiuMedical Diagnostic Centre, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Xingpeng ZhaoMedical Diagnostic Centre, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Yawei LiDepartment of Orthopedics, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China. nianxiang0301@126.com.
Luoyang Central Hospital Affiliated to Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNAs (miRNAs) play essential roles in progression of hepatocellular carcinoma (HCC). However, the roles of miR-196a and miR-196b as well as mechanism in HCC progression remain poorly understood. The expressions of miR-196a, miR-196b and suppressor of cytokine signaling 2 (SOCS2) were measured in HCC tissues and cells by quantitative real-time polymerase chain reaction or immunohistochemistry. HCC progression was investigated by cell proliferation, glycolysis, cycle, clones, apoptosis, and necrosis. The interaction between SOCS2 and miR-196a or miR-196b was explored by luciferase activity and RNA immunoprecipitation analyses. The expressions of proteins in Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway were measured by western blot. A xenograft model was established to investigate the roles of miR-196a or miR-196b in vivo. We found that miR-196a and miR-196b were highly expressed in HCC tissues and cells. High expression of miR-196a or miR-196b was correlated with tumor size, tumor-node-metastasis stage, lymph node metastasis, albumin-bilirubin grade and poor 5-year survival. Knockdown of miR-196a or miR-196b suppressed cell proliferation, glycolysis, cell cycle process, colony formation but induced apoptosis or necrosis in HCC cells. SOCS2 was targeted by miR-196a and miR-196b and its interference ablated abrogation of miR-196a or miR-196b-mediated inhibitory effect on HCC progression. SOCS2 was negatively associated with activation of the JAK/STAT pathway. Besides, knockdown of miR-196a or miR-196b limited xenograft tumor growth by blocking the JAK/STAT pathway. We concluded that downregulation of miR-196a or miR-196b inhibited HCC progression through regulating the JAK/STAT pathway via targeting SOCS2, providing novel targets for prognosis and therapeutics of HCC.

Indexed as

AnimalsAntagomirsApoptosisCarcinoma, HepatocellularCell Line, TumorFemaleHumansJanus KinasesKaplan-Meier EstimateLiver NeoplasmsMaleMiceMice, NudeMicroRNAsMiddle AgedRNA InterferenceAntagomirsJanus KinasesMicroRNAsMIRN196 microRNA, humanRNA, Small InterferingSOCS2 protein, humanSTAT Transcription FactorsSuppressor of Cytokine Signaling Proteins

Identifiers

PMID30988277
PMCPMC6465376
OpenAlexW2940291779

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.