Molecular changes associated with the anticancer effect of sulforaphane against Ehrlich solid tumour in mice

The anticancer effect of sulforaphane (SFN) is mediated by several signalling pathways. However, little is known regarding the underlying mechanism in Ehrlich solid tumours (ESTs) in mice. This study was conducted to determine molecular changes associated with the anticancer effect of SFN and to com...

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Bibliographic Details
Published in:Journal of biochemical and molecular toxicology 2021-02, Vol.35 (2), p.e22655-n/a
Main Authors: Abouzed, Tarek K., Beltagy, Esraa‐Elden R., Kahilo, Khaled A., Ibrahim, Wafaa M.
Format: Article
Language:English
Subjects:
Adenocarcinoma
Anticancer properties
Cancer
Cyclooxygenase-2
DNMT1 protein
Ehrlich solid tumour
Epigenetics
Gene expression
Genes
Inflammation
NF-κB protein
NRF2 protein
Oxidative stress
Polymerase chain reaction
Signal transduction
Solid tumors
Sulforaphane
Tumors
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Summary:The anticancer effect of sulforaphane (SFN) is mediated by several signalling pathways. However, little is known regarding the underlying mechanism in Ehrlich solid tumours (ESTs) in mice. This study was conducted to determine molecular changes associated with the anticancer effect of SFN and to compare its preventive (cotreatment) and therapeutic (posttreatment) effects. Ehrlich (murine mammary adenocarcinoma) solid tumour was selected and changes in the gene expression were determined in tumour tissues by the real‐time polymerase chain reaction. The results showed that SFN increased the expression of the oxidative stress gene NrF2 and its downstream targets (HO1 and CAT). Conversely, SFN administration decreased the expression of the epigenesis‐related genes (HDAC1 and DNMT1) and inflammation‐related genes (TNFa, NFkB and Cox2). Overall, SFN cotreatment presented notable molecular changes than the posttreatment strategy. These data suggest that molecular changes associated with the anticancer effects of SFN against EST involved induction of oxidative stress, inhibition of inflammation and epigenetic modifications.
ISSN:1095-6670
1099-0461
DOI:10.1002/jbt.22655