Heme oxygenase-1 & 2 and their potential contribution in heme induced colorectal carcinogenesis.

Autor: Gamage SMK; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia; Department of Anatomy, Faculty of Medicine, University of Peradeniya, Peradeniya 20404, Sri Lanka., Nanayakkara S; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia., Macfarlane L; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia., Hewage D; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia., Cheng T; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia., Aktar S; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia; Department of Biochemistry and Molecular Biology, Mawlana Bhashani Science and Technology University, Tangail 1902, Bangladesh., Lu CT; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia., Dissabandara L; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia., Islam F; Department of Biochemistry and Molecular Biology, University of Rajshahi, Rajshahi 6205, Bangladesh., Lam AK; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia. Electronic address: a.lam@griffith.edu.au., Gopalan V; Cancer Molecular Pathology, School of Medicine, Griffith University, Gold Coast, Queensland 4222, Australia. Electronic address: v.gopalan@griffith.edu.au.
Jazyk: angličtina
Zdroj: Pathology, research and practice [Pathol Res Pract] 2022 May; Vol. 233, pp. 153885. Date of Electronic Publication: 2022 Apr 07.
DOI: 10.1016/j.prp.2022.153885
Abstrakt: Background: Literature suggests Heme oxygenase (HO) system to be a double-edged sword which can promote both cytoprotection as well as carcinogenicity. The aim of this study was to investigate the role of heme in HO-1 and HO-2 induced colorectal carcinogenesis and the clinicopathological significance of their expressions in patients with colorectal carcinoma (CRC).
Methods: HO-1 and HO-2 expression alterations in normal colonic epithelial (FHC) and colon cancer cells (SW480) were explored following treatment with 0 µM, 25 µM, 100 µM and 250 µM concentrations of hemin, using qPCR. Fifty paired CRC and adjacent non-neoplastic samples were subjected to qPCR to determine the HO-1 and HO-2 expression. Clinicopathological associations of HO-1 and HO-2 expression levels were determined.
Results: Low concentrations of hemin caused upregulation and high concentration caused downregulation of HO-1 expression, whereas HO-2 expression was significantly downregulated with all hemin concentrations in FHC. HO-1 expression in SW480 was increased with all hemin concentrations and HO-2 expression was downregulated at the highest hemin concentration. HO-1 and HO-2 expressions in adjacent non-neoplastic tissue was significantly higher than that of CRC. Expression of HO-1 was significantly higher than HO-2, in both CRC and adjacent non-neoplastic tissue. Sex, HFE expression and lymph-vascular invasion were significantly correlated with HO-1 expression. HO-2 expression showed significant associations with staging, local spread and recurrence of tumour.
Conclusion: HO-1 and HO-2 expression is respectively induced and repressed by exogenous hemin in normal colon and colon cancer cells. HO-1 and HO-2 expression profiles in CRC are correlated with the assessed clinicopathological features of CRC, suggesting the possible implications of HO expression status in CRC pathogenesis.
(Copyright © 2022 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
Externí odkaz: