Ubc9 Attenuates Myocardial Ischemic Injury Through Accelerating Autophagic Flux

Xiao, Qing; Chen, Xiu-Hui; Jiang, Ru‐Chao; Chen, Sheng‑Ying; Chen, Kai-Feng; Zhu, Xiang Yang; Huang, Junjun; Qin, Yuan; Zhang, Guiping; Quan, Yi; Luo, Jia

doi:10.3389/fphar.2020.561306

Cited by 12 publications

(11 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increasing evidence has shown that bafilomycin A1 could hinder the degradation of p62 25,26 and potentially elevate LC3 B accumulation. 27,28 These were consistent with the results above. Therefore, p62 degradation was inhibited in SGC-7901 and SGC-7901/DDP cells, indicating that bafilomycin A1 had suppressed cell autophagy effectively.…”

Section: ■ Resultssupporting

confidence: 92%

Effects and Mechanisms of Saikosaponin D Improving the Sensitivity of Human Gastric Cancer Cells to Cisplatin

Shi

et al. 2021

ACS Omega

View full text Add to dashboard Cite

Gastric cancer (GC) is the second leading cause of cancer deaths around the world. Chemoresistance is an important reason for poor prognosis of GC. Saikosaponin D (SSD) is a natural constituent from Radix Bupleuri and exhibits various activities including antitumors. This study investigated the effects and the mechanisms of SSD on cisplatin (cis-diamminedichloroplatinum, DDP) sensitivity of GC cells. Findings suggested that SSD could promote the inhibitory effect of DDP on proliferation and invasion and increase DDP-induced apoptosis in SGC-7901 and DDP-resistant cell line SGC-7901/DDP. We further identified that SSD increased levels of LC3 B and cleaved caspase 3 and decreased levels of p62, IKK β, p-IκB α, and NF-κB p65, suggesting that SSD might inhibit the IKK β/NF-κB pathway and induce both cell autophagy and apoptosis in SGC-7901 and SGC-7901/DDP. A further study indicated that SSD enhanced the effect of DDP-induced cleaved caspase 3 level rise and NF-κB pathway suppression, especially in SGC-7901/DDP cells. Conclusively, SSD enhanced DDP sensitivity of GC cells; the potential molecular mechanisms were that SSD-induced apoptosis and autophagy and inhibited the IKK β/NF-κB pathway in GC cells. These findings suggested that SSD might contribute to overcoming DDP resistance in GC treatment.

show abstract

Section: ■ Resultssupporting

confidence: 92%

Effects and Mechanisms of Saikosaponin D Improving the Sensitivity of Human Gastric Cancer Cells to Cisplatin

Shi

et al. 2021

ACS Omega

View full text Add to dashboard Cite

show abstract

“…81 Ubc9 levels were increased after myocardium ischemia in mice, and the administration of a Ubc9-expressing adenovirus directly to the infarct area of the heart, to further increase Ubc9 levels in the damaged area, reduced cardiomyocyte apoptosis and fibrosis, and improved cardiac function. 71 This improvement was also attributed to the enhancement of the autophagic influx, which facilitates cell restoration against starvation and other stresses. 84 Xiao et al 71 reported that although the basal levels of Vps34, a member of Class III phosphatidylinositol 3-kinase (PI3K) that regulates cell homeostasis and autophagy, did not change, SUMOylation seemed to regulate the interaction of Vps34 and other factors, such as Beclin1, which enhance the autophagic influx.…”

Section: Heartmentioning

confidence: 99%

“…71 This improvement was also attributed to the enhancement of the autophagic influx, which facilitates cell restoration against starvation and other stresses. 84 Xiao et al 71 reported that although the basal levels of Vps34, a member of Class III phosphatidylinositol 3-kinase (PI3K) that regulates cell homeostasis and autophagy, did not change, SUMOylation seemed to regulate the interaction of Vps34 and other factors, such as Beclin1, which enhance the autophagic influx. Bian et al 70 demonstrated that ischemia/reperfusion injury reduced SUMOylated proteins and Ubc9 expression; however, supplementation with zinc prevented Ubc9 decrease, improved the SUMO1-ylation of DRP-1induced mitophagy, enhanced damaged mitochondrial clearance, and decreased ROS.…”

Section: Heartmentioning

confidence: 99%

SUMOylation in peripheral tissues under low perfusion‐related pathological states

Oliveira

Soares

Harms

et al. 2022

J of Cellular Biochemistry

View full text Add to dashboard Cite

SUMOylation is described as a posttranslational protein modification (PTM) that is involved in the pathophysiological processes underlying several conditions related to ischemia‐ and reperfusion‐induced damage. Increasing evidence suggests that, under low oxygen levels, SUMOylation might be part of an endogenous mechanism, which is triggered by injury to protect cells within the central nervous system. However, the role of ischemia‐induced SUMOylation in the periphery is still unclear. This article summarizes the results of recent studies regarding SUMOylation profiles in several diseases characterized by impaired blood flow to the cardiorenal, gastrointestinal, and respiratory systems. Our review shows that although ischemic injury per se does not always increase SUMOylation levels, as seen in strokes, it seems that in most cases the positive modulation of protein SUMOylation after peripheral ischemia might be a protective mechanism. This complex relationship warrants further investigation, as the role of SUMOylation during hypoxic conditions differs from organ to organ and is still not fully elucidated.

show abstract

“…AML cells transfected with the SUMOylation motif of IGF-1R mutants (K1025A and K1100A) result in decreased cell proliferation by IGF-1 [ 141 ]. Ubiquitin conjugating enzyme 9 (UBC9) is a SUMO E2-conjugation enzyme and plays a critical role in SUMOylation [ 142 ]. Inhibition of UBC9 using an anti-UBC9 antibody reduces the expressions of IGF-1R and SUMO-1, with subsequent inhibition of cell proliferation [ 141 ].…”

Section: Sumoylation In Amlmentioning

confidence: 99%

“…This inhibitory effect promotes apoptosis but does not affect the differentiation of APL cells [ 167 ]. Conversely, upregulated UBP43 expression stabilizes PML/RARα protein and inhibits apoptosis [ 142 ].…”

Section: Deisgylation In Amlmentioning

confidence: 99%

Acute Myeloid Leukemia-Related Proteins Modified by Ubiquitin and Ubiquitin-like Proteins

Park

Baek

2022

IJMS

View full text Add to dashboard Cite

Acute myeloid leukemia (AML), the most common form of an acute leukemia, is a malignant disorder of stem cell precursors of the myeloid lineage. Ubiquitination is one of the post-translational modifications (PTMs), and the ubiquitin-like proteins (Ubls; SUMO, NEDD8, and ISG15) play a critical role in various cellular processes, including autophagy, cell-cycle control, DNA repair, signal transduction, and transcription. Also, the importance of Ubls in AML is increasing, with the growing research defining the effect of Ubls in AML. Numerous studies have actively reported that AML-related mutated proteins are linked to Ub and Ubls. The current review discusses the roles of proteins associated with protein ubiquitination, modifications by Ubls in AML, and substrates that can be applied for therapeutic targets in AML.

show abstract

Ubc9 Attenuates Myocardial Ischemic Injury Through Accelerating Autophagic Flux

Abstract: Aims: SUMOylation is a post-translational modification that plays a crucial role in the cellular stress response. We aimed to demonstrate whether and how the SUMO E2 conjugation enzyme Ubc9 affects acute myocardial ischemic (MI) injury.

Cited by 12 publications

References 42 publications

Effects and Mechanisms of Saikosaponin D Improving the Sensitivity of Human Gastric Cancer Cells to Cisplatin

Effects and Mechanisms of Saikosaponin D Improving the Sensitivity of Human Gastric Cancer Cells to Cisplatin

SUMOylation in peripheral tissues under low perfusion‐related pathological states

Acute Myeloid Leukemia-Related Proteins Modified by Ubiquitin and Ubiquitin-like Proteins

Contact Info

Product

Resources

About