The E3 ubiquitin-protein ligase Rbx1 regulates cardiac wall morphogenesis in zebrafish

Sarvari, Pourya; Rasouli, S. Javad; Allanki, Srinivas; Stone, Oliver A.; Sokòl, Anna M.; Graumann, Johannes; Stainier, Didier Y.R.

doi:10.1016/j.ydbio.2021.07.019

Cited by 4 publications

(8 citation statements)

References 62 publications

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“…RBX1 is a critical component of the E3 ubiquitin ligase [ 30 ]. Considering its evolution, it is conserved in both yeast and humans and exerts a significant role in embryonic development.…”

Section: Discussionmentioning

confidence: 99%

“…Considering its evolution, it is conserved in both yeast and humans and exerts a significant role in embryonic development. In recent years, it has been shown that RBX1 exerts a major role in the modulation of several cellular physiological functions and is simultaneously associated with carcinogenesis [ 30 ]. In several primary tumors, including lung cancer, non-muscle invasive bladder transitional cell carcinoma (NMIBC), and liver cancer, RBX1 is overexpressed.…”

Section: Discussionmentioning

confidence: 99%

“…Post-translational modification of E3 ubiquitin ligase can regulate the function, fate, and intracellular mechanism of the target proteins [ 38 ]. RBX1 interacts with multiple substrates to play a key role [ 30 , 39 ]. Ubiquitin proteasome-mediated SMAR1 degradation is the key mechanism that regulates SMAR1 levels in cells.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, it has been shown that RBX1 is a major regulator of the ubiquitin–proteasome system (UPS) in cancer [ 28 , 29 ]. RBX1 facilitates the target protein ubiquitination carried out by ubiquitin ligase E3 and tags proteins for degradation [ 27 , 30 ]. However, the exact role of RBX1 in ATC progression and the potential signaling cascade is still uncertain.…”

Section: Introductionmentioning

confidence: 99%

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RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex

Yang

et al. 2023

Cell Biosci

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Background Anaplastic thyroid carcinoma (ATC) is one of the most aggressive malignancies, frequently accompanied by metastasis and aerobic glycolysis. Cancer cells adjust their metabolism by modulating the PKM alternative splicing and facilitating PKM2 isoform expression. Therefore, identifying factors and mechanisms that control PKM alternative splicing is significant for overcoming the current challenges in ATC treatment. Results In this study, the expression of RBX1 was largely enhanced in the ATC tissues. Our clinical tests suggested that high RBX1 expression was significantly related to poor survival. The functional analysis indicated that RBX1 facilitated the metastasis of ATC cells by enhancing the Warburg effect, and PKM2 played a key role in RBX1-mediated aerobic glycolysis. Furthermore, we confirmed that RBX1 regulates PKM alternative splicing and promotes the PKM2-mediated Warburg effect in ATC cells. Moreover, ATC cell migration and aerobic glycolysis induced by RBX1-mediated PKM alternative splicing are dependent on the destruction of the SMAR1/HDAC6 complex. RBX1, as an E3 ubiquitin ligase, degrades SMAR1 in ATC through the ubiquitin–proteasome pathway. Conclusion Overall, our study identified the mechanism underlying the regulation of PKM alternative splicing in ATC cells for the first time and provides evidence about the effect of RBX1 on cellular adaptation to metabolic stress.

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“…RBX1 is a critical component of the E3 ubiquitin ligase [ 30 ]. Considering its evolution, it is conserved in both yeast and humans and exerts a significant role in embryonic development.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex

Yang

et al. 2023

Cell Biosci

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“…Moreover, it has been the leading tool for the production of genome-engineered crops [ 281 ]. So far, TALEN has been used in multiple biological studies to produce targeted mutations across different species [ 282 , 283 , 284 , 285 ]. TALEN can be delivered as protein, as RNA, or as DNA, and can be transferred to a living cell or to an organism through different methods depending on the goal of the project and the recipient organism: (1) physical methods: microinjection and electroporation, (2) viral delivery, (3) bacterial delivery, and (4) chemical methods: liposomes or PEG [ 286 ].…”

Section: Future Perspectives and Novel Strategies For Breast Cancermentioning

confidence: 99%

Advances of Epigenetic Biomarkers and Epigenome Editing for Early Diagnosis in Breast Cancer

Sarvari

Ramírez-Díaz

et al. 2022

IJMS

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Epigenetic modifications are known to regulate cell phenotype during cancer progression, including breast cancer. Unlike genetic alterations, changes in the epigenome are reversible, thus potentially reversed by epi-drugs. Breast cancer, the most common cause of cancer death worldwide in women, encompasses multiple histopathological and molecular subtypes. Several lines of evidence demonstrated distortion of the epigenetic landscape in breast cancer. Interestingly, mammary cells isolated from breast cancer patients and cultured ex vivo maintained the tumorigenic phenotype and exhibited aberrant epigenetic modifications. Recent studies indicated that the therapeutic efficiency for breast cancer regimens has increased over time, resulting in reduced mortality. Future medical treatment for breast cancer patients, however, will likely depend upon a better understanding of epigenetic modifications. The present review aims to outline different epigenetic mechanisms including DNA methylation, histone modifications, and ncRNAs with their impact on breast cancer, as well as to discuss studies highlighting the central role of epigenetic mechanisms in breast cancer pathogenesis. We propose new research areas that may facilitate locus-specific epigenome editing as breast cancer therapeutics.

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Emerging Roles of Cullin-RING Ubiquitin Ligases in Cardiac Development

Zambrano-Carrasco,

Zou,

Wang

et al. 2024

Cells

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Heart development is a spatiotemporally regulated process that extends from the embryonic phase to postnatal stages. Disruption of this highly orchestrated process can lead to congenital heart disease or predispose the heart to cardiomyopathy or heart failure. Consequently, gaining an in-depth understanding of the molecular mechanisms governing cardiac development holds considerable promise for the development of innovative therapies for various cardiac ailments. While significant progress in uncovering novel transcriptional and epigenetic regulators of heart development has been made, the exploration of post-translational mechanisms that influence this process has lagged. Culling-RING E3 ubiquitin ligases (CRLs), the largest family of ubiquitin ligases, control the ubiquitination and degradation of ~20% of intracellular proteins. Emerging evidence has uncovered the critical roles of CRLs in the regulation of a wide range of cellular, physiological, and pathological processes. In this review, we summarize current findings on the versatile regulation of cardiac morphogenesis and maturation by CRLs and present future perspectives to advance our comprehensive understanding of how CRLs govern cardiac developmental processes.

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The E3 ubiquitin-protein ligase Rbx1 regulates cardiac wall morphogenesis in zebrafish

Cited by 4 publications

References 62 publications

RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex

RBX1 regulates PKM alternative splicing to facilitate anaplastic thyroid carcinoma metastasis and aerobic glycolysis by destroying the SMAR1/HDAC6 complex

Advances of Epigenetic Biomarkers and Epigenome Editing for Early Diagnosis in Breast Cancer

Emerging Roles of Cullin-RING Ubiquitin Ligases in Cardiac Development

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