RETRACTED ARTICLE: F-box and WD repeat domain-containing 7 (FBXW7) mediates the hypoxia inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway to affect hypoxic-ischemic brain damage in neonatal rats

Sun, Ling

doi:10.1080/21655979.2021.2011635

Cited by 6 publications

(5 citation statements)

References 51 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our finding that the expression of the vasoactive and neurotrophic factor VEGF-A was transiently increased after acute hypoxia is consistent with previous observations by our group [ 5 ] and others [ 33 ] and represents a characteristic compensatory response of the developing brain to hypoxia [ 3 ]. However, the dual functions of VEGF-A in the acute period of cerebral hypoxia prevent a coherent estimation of this response to HI and depend on the degree of hypoxia and time [ 34 , 35 ].…”

Section: Discussionsupporting

confidence: 93%

Further Evidence of Neuroprotective Effects of Recombinant Human Erythropoietin and Growth Hormone in Hypoxic Brain Injury in Neonatal Mice

Klepper

Jung

Dittmann

et al. 2022

IJMS

View full text Add to dashboard Cite

Experimental in vivo data have recently shown complementary neuroprotective actions of rhEPO and growth hormone (rhGH) in a neonatal murine model of hypoxic brain injury. Here, we hypothesized that rhGH and rhEPO mediate stabilization of the blood–brain barrier (BBB) and regenerative vascular effects in hypoxic injury to the developing brain. Using an established model of neonatal hypoxia, neonatal mice (P7) were treated i.p. with rhGH (4000 µg/kg) or rhEPO (5000 IU/kg) 0/12/24 h after hypoxic exposure. After a regeneration period of 48 h or 7 d, cerebral mRNA expression of Vegf-A, its receptors and co-receptors, and selected tight junction proteins were determined using qRT-PCR and ELISA. Vessel structures were assessed by Pecam-1 and occludin (Ocln) IHC. While Vegf-A expression increased significantly with rhGH treatment (p < 0.01), expression of the Vegfr and TEK receptor tyrosine kinase (Tie-2) system remained unchanged. RhEPO increased Vegf-A (p < 0.05) and Angpt-2 (p < 0.05) expression. While hypoxia reduced the mean vessel area in the parietal cortex compared to controls (p < 0.05), rhGH and rhEPO prevented this reduction after 48 h of regeneration. Hypoxia significantly reduced the Ocln+ fraction of cortical vascular endothelial cells. Ocln signal intensity increased in the cortex in response to rhGH (p < 0.05) and in the cortex and hippocampus in response to rhEPO (p < 0.05). Our data indicate that rhGH and rhEPO have protective effects on hypoxia-induced BBB disruption and regenerative vascular effects during the post-hypoxic period in the developing brain.

show abstract

Section: Discussionsupporting

confidence: 93%

Further Evidence of Neuroprotective Effects of Recombinant Human Erythropoietin and Growth Hormone in Hypoxic Brain Injury in Neonatal Mice

Klepper

Jung

Dittmann

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…For instance, in breast cancer cells, it has been verified that Parkin acts as a tumor suppressor [ 175 ] via ubiquitinating HIF-1α on Lys-477 site. Moreover, MDM2 [ 176 ], TRAF6 [ 177 ], FBXW7 [ 178 ], and FBOX11 [ 179 ] could also stimulate the ubiquitination of HIF-1α in human CRC, glioblastoma, and lung cancer.…”

Section: The Ups Links Oncogenic Signal Pathways In Cancer Metabolismmentioning

confidence: 99%

The Ubiquitin–Proteasome System in Tumor Metabolism

Wang

Xiang

Fan

et al. 2023

Cancers

View full text Add to dashboard Cite

Metabolic reprogramming, which is considered a hallmark of cancer, can maintain the homeostasis of the tumor environment and promote the proliferation, survival, and metastasis of cancer cells. For instance, increased glucose uptake and high glucose consumption, known as the “Warburg effect,” play an essential part in tumor metabolic reprogramming. In addition, fatty acids are harnessed to satisfy the increased requirement for the phospholipid components of biological membranes and energy. Moreover, the anabolism/catabolism of amino acids, such as glutamine, cystine, and serine, provides nitrogen donors for biosynthesis processes, development of the tumor inflammatory environment, and signal transduction. The ubiquitin–proteasome system (UPS) has been widely reported to be involved in various cellular biological activities. A potential role of UPS in the metabolic regulation of tumor cells has also been reported, but the specific regulatory mechanism has not been elucidated. Here, we review the role of ubiquitination and deubiquitination modification on major metabolic enzymes and important signaling pathways in tumor metabolism to inspire new strategies for the clinical treatment of cancer.

show abstract

“…Indeed, HIF1-α ubiquitination can be increased also by other ligases, this is the case of FBXW7, which is able to contribute to HIF degradation both in vitro and in vivo [ 63 , 64 , 65 ]. These data strengthen the tumor suppressor role played by FBXW7 in osteosarcoma.…”

Section: Ubiquitinationmentioning

confidence: 99%

Protein Stability Regulation in Osteosarcoma: The Ubiquitin-like Modifications and Glycosylation as Mediators of Tumor Growth and as Targets for Therapy

Di Gregorio,

Di Giuseppe,

Terreri

et al. 2024

Cells

View full text Add to dashboard Cite

The identification of new therapeutic targets and the development of innovative therapeutic approaches are the most important challenges for osteosarcoma treatment. In fact, despite being relatively rare, recurrence and metastatic potential, particularly to the lungs, make osteosarcoma a deadly form of cancer. In fact, although current treatments, including surgery and chemotherapy, have improved survival rates, the disease’s recurrence and metastasis are still unresolved complications. Insights for analyzing the still unclear molecular mechanisms of osteosarcoma development, and for finding new therapeutic targets, may arise from the study of post-translational protein modifications. Indeed, they can influence and alter protein structure, stability and function, and cellular interactions. Among all the post-translational modifications, ubiquitin-like modifications (ubiquitination, deubiquitination, SUMOylation, and NEDDylation), as well as glycosylation, are the most important for regulating protein stability, which is frequently altered in cancers including osteosarcoma. This review summarizes the relevance of ubiquitin-like modifications and glycosylation in osteosarcoma progression, providing an overview of protein stability regulation, as well as highlighting the molecular mediators of these processes in the context of osteosarcoma and their possible targeting for much-needed novel therapy.

show abstract

RETRACTED ARTICLE: F-box and WD repeat domain-containing 7 (FBXW7) mediates the hypoxia inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway to affect hypoxic-ischemic brain damage in neonatal rats

Cited by 6 publications

References 51 publications

Further Evidence of Neuroprotective Effects of Recombinant Human Erythropoietin and Growth Hormone in Hypoxic Brain Injury in Neonatal Mice

Further Evidence of Neuroprotective Effects of Recombinant Human Erythropoietin and Growth Hormone in Hypoxic Brain Injury in Neonatal Mice

The Ubiquitin–Proteasome System in Tumor Metabolism

Protein Stability Regulation in Osteosarcoma: The Ubiquitin-like Modifications and Glycosylation as Mediators of Tumor Growth and as Targets for Therapy

Contact Info

Product

Resources

About