ArticleOncotarget2016
IL-32θ inhibits stemness and epithelial-mesenchymal transition of cancer stem cells via the STAT3 pathway in colon cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Interleukin 32 Expression in Mesothelioma.Thoracic cancer · 2026Article
- Recombinant Human IL-32θ Induces Polarization Into M1-like Macrophage in Human Monocytic Cells.Immune network · 2024Article
- Human IL-32θA94V mutant attenuates monocyte-endothelial adhesion by suppressing the expression of ICAM-1 and VCAM-1 via binding to cell surface receptor integrin αVβ3 and αVβ6 in TNF-α-stimulated HUVECs.Frontiers in immunology · 2023Article
- Comparison of the Seven Interleukin-32 Isoforms' Biological Activities: IL-32θ Possesses the Most Dominant Biological Activity.Frontiers in immunology · 2022Article
- A Paradoxical Effect of Interleukin-32 Isoforms on Cancer.Frontiers in immunology · 2022Review
- The Complex Network between Inflammation and Colorectal Cancer: A Systematic Review of the Literature.Cancers · 2021Review
- Interleukin-32θ Triggers Cellular Senescence and Reduces Sensitivity to Doxorubicin-Mediated Cytotoxicity in MDA-MB-231 Cells.International journal of molecular sciences · 2021Article
- Clinical Implications of Colorectal Cancer Stem Cells in the Age of Single-Cell Omics and Targeted Therapies.Gastroenterology · 2021Review
- IL-32 induces epithelial-mesenchymal transition by triggering endoplasmic reticulum stress in A549 cells.BMC pulmonary medicine · 2020Article
- Local and Systemic Interleukin-32 in Esophageal, Gastric, and Colorectal Cancers: Clinical and Diagnostic Significance.Diagnostics (Basel, Switzerland) · 2020Article
- Apatinib ameliorates doxorubicin-induced migration and cancer stemness of osteosarcoma cells by inhibiting Sox2 via STAT3 signalling.Journal of orthopaedic translation · 2020Article
- Review
- Hypoxia-induced secretion stimulates breast cancer stem cell regulatory signalling pathways.Molecular oncology · 2019Article
- IL-32γ suppresses lung cancer stem cell growth via inhibition of ITGAV-mediated STAT5 pathway.Cell death & disease · 2019Article
- Interleukin-32θ inhibits tumor-promoting effects of macrophage-secreted CCL18 in breast cancer.Cell communication and signaling : CCS · 2019Article
- ENO1 Acts as a Prognostic Biomarker Candidate and Promotes Tumor Growth and Migration Ability Through the Regulation of Rab1A in Colorectal Cancer.Cancer management and research · 2019Article
- Inhibition of skin carcinogenesis by suppression of NF-κB dependent ITGAV and TIMP-1 expression in IL-32γ overexpressed condition.Journal of experimental & clinical cancer research : CR · 2018Article
- STK899704 inhibits stemness of cancer stem cells and migration via the FAK-MEK-ERK pathway in HT29 cells.BMB reports · 2018Article
- Role of interleukin-32 in cancer biology.Oncology letters · 2018Review
- Protein tyrosine phosphatase receptor-type δ acts as a negative regulator suppressing breast cancer.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-32 is a well-known cytokine associated with inflammation, virus infections and cancer. IL-32θ is a newly identified isoform of IL-32, whose function has yet to be elucidated. In this study, we investigated IL-32θ function in colon cancer stem cells. Using samples from colon cancer patients, we found that the expression of IL-32θ mRNAs was significantly suppressed in tumor regions. We investigated the effects of IL-32θ on colon cancer. Ectopic expression of IL-32θ attenuated invasion, migration in vitro and in vivo tumorigenicity of colon cancer cells. IL-32θ inhibited epithelial-mesenchymal transition (EMT), resulting in the suppression of their migratory and invasive capabilities of HT29 colon cancer cells. In addition, IL-32θ altered various properties of CSCs, including sphere formation and expression of stemness related genes. IL-32θ directly bound to STAT3 and inhibited its nuclear translocation, leading to inhibited transcription of downstream factors, including Bmi1 and ZEB1. We showed that IL-32θ inhibited the STAT3-ZEB1 pathway and consequently inhibited key factors of stemness and EMT. Taken together, our findings reveal that IL-32θ can be a tumor suppressor, indicating that IL-32θ could possibly be used in therapies for colon cancer.
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