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. 2022 Jan 31;21:15330338211065252. doi: 10.1177/15330338211065252

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© The Author(s) 2022

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 7. — Mechanism diagram for interaction between bortezomib and cyclin D1 is displayed in the figure below. Bortezomib can regulate expression of cyclin D1 by inhibiting the activity of NF- κB and down-regulating expression of EIF4EmRNA to reduce expression of CCND1mRNA. Cyclin D1/CDK4 activity plays an important role in the induction of NOXA protein, thus directly enhancing the anti-tumor effect of bortezomib. Besides, cyclin D1 can enhance the effect of bortezomib on PERK/CHOP axis and activate unfolded protein response (UPR) to induce the apoptosis pathway of bortezomib through endoplasmic reticulum (ER) stress.

Abbreviations: NF-κB, nuclear factor kappa-B; EIF4E, eukaryotic initiation factor 4E; NOXA, A BH3-only member of Bcl-2; AKT, protein kinase B; PERK, PKR-like ER kinase; CHOP, C/EBP-homologous protein; UPR, unfolded protein response; ER, endoplasmic reticulum; Rb, retinoblastoma gene; E2F, the E2F family of DNA-binding transcription factors; P, phosphoric acid.