Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related death. Cytokines, including interleukin 24 (IL-24), play an important role in HCC. IL-24 inhibits HCC metastasis but the molecular mechanism by which this occurs is still unknown. MicroRNAs (miRNAs) are regulators of cancers including hepatocellular carcinoma (HCC). However, the role that miRNAs play in the regulation of IL-24 in HCC is unclear. The aim of this study was to investigate the effects of regulation of IL-24 by miR-203a-3p.1 on liver cancer cell proliferation and metastasis. IL-24 mRNA and miR-203a-3p.1 were detected by real-time RT-PCR, and IL-24 protein in the cell growth medium was measured by ELISA. A luciferase assay was used to verify that the IL-24 gene was the target of miR-203a-3p.1. Cell survival ability was detected by the MTT assay and colony formation. Cell metastasis was assayed by the Transwell system. The results showed that IL-24 could be down-regulated by miR-203a-3p.1 in HCC cells and that miR-203a-3p.1 acted as an onco-miRNA by targeting IL-24. Inhibition of miR-203a-3p.1 in cells could lead to the reversal of HCC cell proliferation and metastasis. The study highlights a novel molecular interaction between miR-203a-3p.1 and IL-24, which indicates that IL-24 and miR-203a-3p.1 may constitute potential therapeutic targets for HCC.
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http://dx.doi.org/10.1002/2211-5463.12248 | DOI Listing |
Toxicol Appl Pharmacol
December 2024
College of Medicine, Graduate School, Kyung Hee University, 02447, Republic of Korea; Division of Cardiology, Department of Internal Medicine, Kyung-Hee University Hospital, Kyung Hee University, 02447, Republic of Korea. Electronic address:
In the current study, we dosed Didecyldimethylammonium chloride (DDAC) in mice by pharyngeal aspiration for 28 days or 90 days (weekly) and tried to elucidate the relationship between lamellar body formation and the lesions. When exposed for 28 days (0, 5, 10, 50, and 100 μg/head), all the mice in the 50 and 100 μg/head groups died since Day 2 after the third dosing (Day 16 after the first dosing). Edema, necrosis of bronchiolar and alveolar epithelium, and fibrinous exudate were observed in the lungs of all the dead mice, and chronic inflammatory lesions were observed in the lung tissues of alive mice.
View Article and Find Full Text PDFActa Pharm Sin B
November 2024
Shanghai Frontiers Science Center of Drug Target Identification and Delivery, National Key Laboratory of Innovative Immunotherapy, School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, China.
Immunocytokines, employing targeted antibodies to concentrate cytokines at tumor sites, have shown potential advantages such as prolonged cytokine half-lives, mitigated adverse effects, and synergistic antitumor efficacy from both antibody and cytokine components. First, we present an in-depth analysis of the advancements of immunocytokines evaluated in preclinical and clinical applications. Notably, anti-PD-1-based immunocytokines can redirect cytokines to intratumoral CD8 T cells and reinvigorate them to elicit robust antitumor immune responses.
View Article and Find Full Text PDFRhinology
December 2024
Center of Allergy and Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health, Germany, Member of the German Center for Lung Research (DZL), Munich, Germany and Member of the Helmholtz I and I Initiative.
Background: Allergen-specific immunotherapy (AIT) is a disease-modifying therapy and is effective to reduce the symptoms of grass pollen-allergy. The airway epithelium of these patients releases inflammatory mediators including type-2 cytokines, which are associated with cellular processes involved in the symptomatic response of the affected tissue. Aim of the study was to identify epithelial biomarkers indicating AIT progress.
View Article and Find Full Text PDFJ Eur Acad Dermatol Venereol
December 2024
The Second Affiliated Hospital of Xi' an Jiaotong University, Xi'an, Shaanxi, China.
Unlabelled: While autoantibodies in bullous pemphigoid (BP) are known to activate the innate immune response, their direct effect on keratinocytes, and the contribution of BP-IgG autoantibody-dependent keratinocyte responses to BP pathology is largely unknown. Herein, we performed multiplex immunoassays and bulk RNA-seq on primary keratinocytes treated with IgG from BP patients or controls. We identified a pro-inflammatory and proteolytic response with release of several cytokines (IL-6, IL-24, TGF-β1), chemokines (CXCL16, CTACK, MIP-3β, RANTES), C1s, DPP4, and MMP-9.
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