Evidence map›Paper›PMID 26467022›Full record

ArticleCancer biology & therapy2015

microRNA-622 acts as a tumor suppressor in hepatocellular carcinoma.

Wei-Hua Song, Xiao-Jun Feng, Shao-Juan Gong, Jian-Ming Chen, Shou-Mei Wang, Dong-Juan Xing, Ming-Hua Zhu, Shu-Hui Zhang, Ai-Min Xu

Abstract read
In one paragraph

Article in Cancer biology & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
–field-weighted citation impact
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

26 citing papers in PubMed.

  1. Article
  2. miRNAs in HCC, pathogenesis, and targets.Hepatology (Baltimore, Md.) · 2024
    Article
  3. Wogonin inhibits hepatoma cell proliferation by targeting miR-27b-5p/YWHAZ axis.Journal of biochemical and molecular toxicology · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Tumor Suppressor microRNAs in Gastrointestinal Cancers: A Mini-Review.Recent advances in inflammation & allergy drug discovery · 2022
    Review
  8. Review
  9. Article
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  11. 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

9 authors.

Wei-Hua Songa Department of Interventional Oncology ; Renji Hospital; School of Medicine; Shanghai Jiao Tong University ; Shanghai , China.
Xiao-Jun Fengb Department of Pathology ; Yueyang Hospital; Shanghai University of Traditional Chinese Medicine ; Shanghai , China.
Shao-Juan Gonga Department of Interventional Oncology ; Renji Hospital; School of Medicine; Shanghai Jiao Tong University ; Shanghai , China.
Jian-Ming Chena Department of Interventional Oncology ; Renji Hospital; School of Medicine; Shanghai Jiao Tong University ; Shanghai , China.
Shou-Mei Wanga Department of Interventional Oncology ; Renji Hospital; School of Medicine; Shanghai Jiao Tong University ; Shanghai , China.
Dong-Juan Xinga Department of Interventional Oncology ; Renji Hospital; School of Medicine; Shanghai Jiao Tong University ; Shanghai , China.
Ming-Hua Zhuc Department of Pathology ; Changhai Hospital and Institute of Liver Diseases; Second Military Medical University ; Shanghai , China.
Shu-Hui Zhangb Department of Pathology ; Yueyang Hospital; Shanghai University of Traditional Chinese Medicine ; Shanghai , China.
Ai-Min Xua Department of Interventional Oncology ; Renji Hospital; School of Medicine; Shanghai Jiao Tong University ; Shanghai , China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNAs (miRNAs) are important regulators of tumor development and progression. In this study, we aimed to explore the expression and role of miR-622 in hepatocellular carcinoma (HCC). We found that miR-622 was significantly downregulated in human HCC specimens compared to adjacent noncancerous liver tissues. miR-622 downregulation was significantly associated with aggressive parameters and poor prognosis in HCC. Enforced expression of miR-622 significantly decreased the proliferation and colony formation and induced apoptosis of HCC cells. In vivo studies demonstrated that miR-622 overexpression retarded the growth of HCC xenograft tumors. Bioinformatic analysis and luciferase reporter assays revealed that miR-622 directly targeted the 3'-untranslated region (UTR) of mitogen-activated protein 4 kinase 4 (MAP4K4) mRNA. Ectopic expression of miR-622 led to a significant reduction of MAP4K4 expression in HCC cells and xenograft tumors. Overexpression of MAP4K4 partially restored cell proliferation and colony formation and reversed the induction of apoptosis in miR-622-overexpressing HCC cells. Inhibition of JNK and NF-κB signaling phenocopied the anticancer effects of miR-622 on HCC cells. Taken together, miR-622 acts as a tumor suppressor in HCC and restoration of miR-622 may provide therapeutic benefits in the treatment of HCC.

Indexed as

Gene Expression Regulation, NeoplasticGenes, Tumor SuppressorAdultAgedAnimalsApoptosisBiomarkersCarcinoma, HepatocellularCell ProliferationDisease Models, AnimalFemaleHumansIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesLiver NeoplasmsMaleBiomarkersIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMAP4K4 protein, humanMicroRNAsMIRN622 microRNA, humanNF-kappa BProtein Serine-Threonine Kinaseshepatocellular carcinomaMAP4K4microRNAmiR-622therapeutic target

Identifiers

PMID26467022
PMCPMC4847826

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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.