Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Aug 7;12(8):2210. doi: 10.3390/cancers12082210

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

A hypothetical model illustrating how FBXL8 attenuates anti-cancer CCND2 and IRF5 factors, upregulates pro-tumorigenic cytokines, suppresses apoptosis and promotes metastasis potential in BRCA. FBXL8, a novel SCF E3 ubiquitin ligase, plays a key role in anti-apoptosis in BRCA. (A) Knockdown of FBXL8 increased expression of cancer suppressors CCND2 and IRF5, thus inhibiting cell growth and proliferation in BRCA, driven by: (i) increase in early apoptosis, (ii) activation of Caspase-9 and -3, and (iii) inhibition of the production of cancer-promoting cytokines, including MCP-1, I-TAC, TECK, CTACK, MIF, GM-CSF, NT-3, FGF-6, Angiogenin, ICAM-1, DtK and EGFR. Therefore, FBXL8 promotes pro-tumorigenic microenvironment, contributing to BRCA metastasis and progression. (B) FBXL8 interacts and downregulates cancer suppressors CCND2 and IRF5 via protein degradation system. Hence, upregulated FBXL8 in BRCA causes the reduction of CCND2 and IRF5 proteins, and leads to dysregulated cell proliferation, immune response and metastatic potential of BRCA cells.

A hypothetical model illustrating how FBXL8 attenuates anti-cancer CCND2 and IRF5 factors, upregulates pro-tumorigenic cytokines, suppresses apoptosis and promotes metastasis potential in BRCA. FBXL8, a novel SCF E3 ubiquitin ligase, plays a key role in anti-apoptosis in BRCA. (A) Knockdown of FBXL8 increased expression of cancer suppressors CCND2 and IRF5, thus inhibiting cell growth and proliferation in BRCA, driven by: (i) increase in early apoptosis, (ii) activation of Caspase-9 and -3, and (iii) inhibition of the production of cancer-promoting cytokines, including MCP-1, I-TAC, TECK, CTACK, MIF, GM-CSF, NT-3, FGF-6, Angiogenin, ICAM-1, DtK and EGFR. Therefore, FBXL8 promotes pro-tumorigenic microenvironment, contributing to BRCA metastasis and progression. (B) FBXL8 interacts and downregulates cancer suppressors CCND2 and IRF5 via protein degradation system. Hence, upregulated FBXL8 in BRCA causes the reduction of CCND2 and IRF5 proteins, and leads to dysregulated cell proliferation, immune response and metastatic potential of BRCA cells.