NFE2L1 and NFE2L3 Complementarily Maintain Basal Proteasome Activity in Cancer Cells through CPEB3-Mediated Translational Repression.
Tsuyoshi Waku,Hiroyuki Katayama,Miyako Hiraoka,Atsushi Hatanaka,Atsushi Hatanaka,Nanami Nakamura,Yuya Tanaka,Natsuko Tamura,Akira Watanabe,Akira Kobayashi +9 more
TLDR
The results provide the novel regulatory mechanism of basal proteasome activity in cancer cells through an NFE2L3-CPEB3-NFE2 L1 translational repression axis and patients with cancer having tumors expressing higher levels of CPEB3/NFE 2L3 exhibit poor prognosis.Abstract:
Proteasomes are protease complexes essential for cellular homeostasis, and their activity is crucial for cancer cell growth. However, the mechanism of how proteasome activity is maintained in cancer cells has remained unclear. The CNC family transcription factor NFE2L1 induces the expression of almost all proteasome-related genes under proteasome inhibition. Both NFE2L1 and its phylogenetically closest homolog, NFE2L3, are highly expressed in several types of cancer, such as colorectal cancer. Here, we demonstrate that NFE2L1 and NFE2L3 complementarily maintain basal proteasome activity in cancer cells. Double knockdown of NFE2L1 and NFE2L3 impaired basal proteasome activity in cancer cells and cancer cell resistance to a proteasome inhibitor anticancer drug, bortezomib, by significantly reducing the basal expression of seven proteasome-related genes: PSMB3, PSMB7, PSMC2, PSMD3, PSMG2, PSMG3, and POMP Interestingly, the molecular basis behind these cellular consequences was that NFE2L3 repressed NFE2L1 translation by the induction of the gene encoding the translational regulator CPEB3, which binds to the NFE2L1 3' untranslated region and decreases polysome formation on NFE2L1 mRNA. Consistent results were obtained from clinical analysis, wherein patients with cancer having tumors expressing higher levels of CPEB3/NFE2L3 exhibit poor prognosis. These results provide the novel regulatory mechanism of basal proteasome activity in cancer cells through an NFE2L3-CPEB3-NFE2L1 translational repression axis.read more
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The transcription factor BACH1 at the crossroads of cancer biology: From epithelial-mesenchymal transition to ferroptosis.
TL;DR: In this article, a two-faced BACH1 model is proposed to explain the dynamic switching between metastasis and stress resistance along with cancer progression, which also brings increased sensitivity to iron-dependent cell death (ferroptosis) through crosstalk of BACH 1 target genes, imposing programmed vulnerability upon cancer cells.
Journal ArticleDOI
Defining the Functional Targets of Cap'n'collar Transcription Factors NRF1, NRF2, and NRF3.
TL;DR: Together, the data provide a quantitative assessment of how NRF family members sculpt proteomes and transcriptomes, providing a framework to understand the critical physiological importance of NRF transcription factors and to establish pharmacologic approaches for therapeutically activating these transcriptional programs in disease.
Journal ArticleDOI
Roles of NRF3 in the Hallmarks of Cancer: Proteasomal Inactivation of Tumor Suppressors
TL;DR: The evidence indicates that NRF3 confers cells with six so-called “hallmarks of cancer”, implying that it exhibits cancer driver gene-like function, and the molecular mechanisms underlyingNRF3 activation have been elucidated.
Journal ArticleDOI
NRF3 upregulates gene expression in SREBP2-dependent mevalonate pathway with cholesterol uptake and lipogenesis inhibition.
Tsuyoshi Waku,Toru Hagiwara,Natsuko Tamura,Yuri Atsumi,Yasuomi Urano,Mikiko Suzuki,Takuya Iwami,Katsuya Sato,Masayuki Yamamoto,Noriko Noguchi,Akira Kobayashi +10 more
TL;DR: In this paper, NRF3 upregulates gene expression in SREBP2-dependent mevalonate pathway, and the expression of the GGPS1 gene encoding an enzyme in the production of farnesyl pyrophosphate (FPP), a lanosterol precursor.
Journal ArticleDOI
Trash Talk: Mammalian Proteasome Regulation at the Transcriptional Level.
TL;DR: The roles of the transcription factors that are involved in the regulation of the mammalian proteasome are highlighted and discussed.
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TL;DR: The height differential between the tallest and shortest populations was 19-20 cm a century ago, and has remained the same for women and increased for men a century later despite substantial changes in the ranking of countries.
Journal ArticleDOI
Increased proteasome-dependent degradation of the cyclin-dependent kinase inhibitor p27 in aggressive colorectal carcinomas.
Massimo Loda,Barry Cukor,Sun W. Tam,Phillip T. Lavin,Michelangelo Fiorentino,Giulio Draetta,J. M. Jessup,Michele Pagano,Michele Pagano +8 more
TL;DR: It was found that carcinomas with low or absent p27 protein displayed enhanced proteolytic activity specific for p27, suggesting that low p27 expression can result from increased proteasome-mediated degradation rather than altered gene expression.