Interleukin-12 treatment reduces tumor growth and modulates the expression of CASKA and MIR-203 in athymic mice bearing tumors induced by the HGC-27 gastric cancer cell line.

Autor: Dellalibera-Joviliano R; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil. Electronic address: redellajov@gmail.com., Garcia ME; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil. Electronic address: medicina@unaerp.br., Marins M; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil; Biotechnology Unit, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., Fachin ALÚ; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil; Biotechnology Unit, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., Couto LB; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., Mesquita E; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil; Syrian Lebanese Hospital, São Paulo, Brazil., Komoto TT; Molecular Oncology Research Center, Barretos Cancer Hospital, Barretos, SP, Brazil., Silva G; Department of Clinical, Toxicological and Bromatological Analysis, Faculty of Pharmaceutical Sciences of Ribeirão Preto-USP, Ribeirão Preto, SP, Brazil., Neto WC; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., Orlando L; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., Durand M; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., França SC; Biotechnology Unit, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil., Bestetti RB; Medicine School, University of Ribeirão Preto, Av. Costábile Romano, Ribeirão Preto, SP 2201, Brazil.
Jazyk: angličtina
Zdroj: Pathology, research and practice [Pathol Res Pract] 2024 Nov; Vol. 263, pp. 155625. Date of Electronic Publication: 2024 Oct 03.
DOI: 10.1016/j.prp.2024.155625
Abstrakt: Gastric cancer (GC) is one of the most common malignant tumors in the digestive system and due to its poor prognosis, there is an increase in the demand for more effective anticancer therapies. Interleukins are potential anticancer agents which can modulate expression of cancer related genes and have therapeutic effects. Interleukin 12 (IL-12) exhibits potent anti-tumor, anti-angiogenic and anti-metastatic activities and represents the ideal candidate for tumor immunotherapy, due to its ability to activate both innate and adaptive immunities. The aim of this study was to evaluate the effect of IL-12 administration on GC tumor growth induced in the cancer xenograft nude mouse model. Tumor development was analyzed weekly and after 8 weeks, the animals were sacrificed for cytokine analysis (IL-4, TNF-alfa, IL-2, INF-gamma, IL-12, IL-10, TGF-beta) by ELISA. The tumor cells in the implanted areas of the animals that developed solid growth of the tumor (anatomopathological analysis was performed). We have also evaluated CASK and miR203 expression, two related cell invasion factors, in the induced tumors after administration of 6 n/kg IL-12. The development of tumor masses was observed in all groups of animals inoculated with HGC-27 neoplastic cells. In animals treated with 6 n/kg IL-12, there was no tumor development confirmed by anatomopathological analysis. Changes in the levels of pro and anti-inflammatory cytokines were also observed. Our results indicated that miR203 expression was elevated while CASK was downregulated. These results suggest that IL-12 treatment repress the tumor growth by induction of miR203 expression which in turn repress CASK expression.
Competing Interests: Declaration of Competing Interest The authors declare that there is no interest.
(Copyright © 2024 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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