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. 2022 Sep 8;13:950109. doi: 10.3389/fphar.2022.950109

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Copyright © 2022 Rahman, Sarker, Alam Tumpa, Yamin, Islam, Park, Islam, Rauf, Sharma, Cavalu and Kim.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Notch signaling pathway. The ligand on the receiving cell connects the cell that acts as a presenter for the notch receptor. ADAM metalloprotease and γ-secretase split the Notch extracellular truncated (NEXT) domain, forming the notch intracellular domain (NICD). NICD is introduced into the nucleus and is a complex of transcription factors CSL 9 CBF1/hairless/lack 1 and transcriptional coactivator of mastermind-like proteins (MAML). The complex would then activate the target gene’s transcription. Treatment with diallyl trisulfide (DATS) boosts the expression of tumor suppressor microRNAs miR-143 and miR-145. When microRNAs bind to Notch1 mRNA, the mRNA is degraded, but the Notch1 protein is not translated. Curcumin inhibits Notch1 transcription and expression and the nucleus’ Hes-1, Hey-1, and Hey-2 genes (Angulo et al., 2017).