Evidence map›Paper›PMID 37264148›Full record

ArticleMolecular biology reports2023

Interleukin-22 promotes the proliferation and migration of hepatocellular carcinoma cells via the phosphoinositide 3-kinase (PI3K/AKT) signaling pathway.

Fizzah Mansur, Tanzeela Arshad, Vaclav Liska, Sobia Manzoor

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. The Role of CD4Cells · 2026
    Review
  2. Article
  3. Review
  4. IL-22/IL-22R1 pathway enhances cholangiocarcinoma progressionWorld journal of gastrointestinal oncology · 2025
    Article
  5. Article
  6. 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

4 authors at 2 institutions in 2 countries.

Fizzah Mansur *Molecular Virology and Immunology Research Group, Atta-Ur-Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad, Pakistan.ORCID http://orcid.org/0000-0002-1844-9696
Tanzeela Arshad *Molecular Virology and Immunology Research Group, Atta-Ur-Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad, Pakistan.ORCID http://orcid.org/0000-0002-6798-0037
Vaclav LiskaDepartment of Surgery, Faculty of Medicine in Pilsen, Charles University, Pilsen, Czechia.
Sobia Manzoor *Molecular Virology and Immunology Research Group, Atta-Ur-Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad, Pakistan. dr.sobiamanzoor@asab.nust.edu.pk.ORCID http://orcid.org/0000-0001-9273-6880
Charles University · CZNational University of Sciences and Technology · PK

Funding

National University of Sciences and Technology, Islamabad, Pakistan Students' Research Funds
6 · The paper itself

Abstract

backgroundInterleukin-22 (IL-22) is a pro-inflammatory cytokine released during the immune response in chronic liver injury. Although IL-22 mediates tissue regeneration, its uncontrolled production may generate a carcinogenic environment resulting in hepatocellular carcinoma (HCC). This study aims to identify the effect of IL-22 on anti-apoptotic and metastatic genes and the molecular pathways responsible for IL-22-mediated hepatic carcinogenesis. METHODS AND

resultsThree cancerous liver lines, HepG2, SNU-387, Huh7, and one normal liver line, THLE2, were treated with IL-22. RT-qPCR analysis was conducted to study the role of IL-22 in altering the expression levels of anti-apoptotic genes, MCL-1 and BCL-2, and metastatic genes, MMP-7 and MMP-9. A significant increase in expression levels of these genes was observed after IL-22 treatment. Furthermore, to explore the major pathways involved in IL-22-mediated upregulation of anti-apoptotic and metastatic genes, cells were treated with inhibitors of JAK/STAT and PI3K/AKT pathways along with IL-22. Resultantly, a significant decrease in expression levels of target genes was observed, indicating the involvement of JAK/STAT and PI3K/AKT signaling cascades in IL-22-mediated oncogenesis. Finally, Cell Scratch assay was performed to check the effect of IL-22 and inhibitors of JAK/STAT and PI3K/AKT on the metastatic potential of liver cells. While migration was observed in Huh7 and THLE2 cells treated with IL-22, no migration was observed in cells treated with IL-22 along with JAK/STAT and PI3K/AKT inhibitors. Results indicate that IL-22 encourages metastasis in HCC cells via the JAK/STAT and PI3K/AKT pathways.

conclusionResults showed that IL-22 upregulates anti-apoptotic and metastatic genes in HCC through JAK/STAT and PI3K/AKT signaling pathways.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsCell Line, TumorCell ProliferationHumansInterleukin-22Phosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionInterleukin-22Phosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktHepatocellular carcinomaIL-22JAK/STAT pathwayPI3K/AKT pathwayProinflammatory cytokine

Identifiers

PMID37264148
OpenAlexW4379093428

What OpenQuestion holds

Textmetadata
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.