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Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE245638 | GEO | 2024/05/03

REPOSITORIES: GEO

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Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation [MWA or MWA+2DG group]

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Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation [MWA+PBS or MWA+2DG]

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Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation

Project description:Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation

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Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation [MWA+PBS or MWA+2DG]

Project description:Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation [MWA+PBS or MWA+2DG]

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Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation [MWA or MWA+2DG group]

Project description:Interfering with glycolysis potentiates the long-term effect of local tumor ablation via CD8+TCM cell differentiation [MWA or MWA+2DG group]

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PTCSC3-mediated glycolysis suppresses thyroid cancer progression via interfering with PGK1 degradation.

Project description:The Warburg effect (aerobic glycolysis), a hallmark of cancer, serves as a promising target for diagnosis and therapy. Growing evidence indicates that long non-coding RNAs (lncRNAs) play an important role in aerobic glycolysis of various tumours. However, the correlation between lncRNAs and glycolysis in thyroid cancer cells is still poorly understood. In this study, we showed that lncRNA papillary thyroid cancer susceptibility candidate 3 (PTCSC3) was significantly downregulated in papillary thyroid carcinoma (PTC). Overexpression of PTCSC3 significantly inhibited the aerobic glycolysis and tumour growth of PTC cells. Consistently, PTCSC3 overexpression suppressed tumour progress in vivo. Mechanistically, PTCSC3 inhibits aerobic glycolysis and proliferation of PTC by directly interacting with PGK1, a key enzyme in glycolytic pathway. As a result, PTCSC3 performs its role in PTC development via PGK1 and may be a potential therapeutic target for PTC treatment.

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Loss of Sirtuin 1 (SIRT1) potentiates endothelial dysfunction via impaired glycolysis during infectious challenge.

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Long-lasting postoperative analgesia with local anesthetic-loaded hydrogels prevent tumor recurrence via enhancing CD8+T cell infiltration

Project description:Postoperative pain (POP) can promote tumor recurrence and reduce the cancer patient's quality of life. However, POP management has always been separated from tumor treatment in clinical practice, and traditional postoperative analgesia using opioids is still unsatisfactory for patients, which is not conducive to tumor treatment. Here, ropivacaine, a popular amide-type LA, was introduced into a Pluronic F127 hydrogel. Postoperative analgesia with ropivacaine-loaded hydrogels reduced the incidence of high-dose ropivacaine-induced convulsions and prolonged pain relief for more than 16 h. More interestingly, ropivacaine-loaded hydrogel was found to upregulate major histocompatibility complex class I (MHC-I) in tumor cells by impairing autophagy. Therefore, a hydrogel co-dopped with ropivacaine and TLR7 agonist imiquimod (PFRM) was rationally synthesized. After postoperative analgesia with PFRM, imiquimod primes tumor-specific CD8+T cells through promoting DCs maturation, and ropivacaine facilitates tumor cells recognition by primed CD8+T cells through upregulating MHC-I. Consequently, postoperative analgesia with PFRM maximumly increases CD8+T cells infiltration into residual tumor tissue and prevents tumor recurrence. Overall, this study for the first time provides an LA-based approach for simultaneous long-lasting postoperative analgesia and prevention of tumor recurrence. Supplementary Information The online version contains supplementary material available at 10.1186/s12951-023-01803-8.

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Long-Term Outcomes of Surgical Ablation for Atrial Fibrillation: Impact of Ablation Lesion Sets.

Project description:BackgroundThe lesion sets for surgical ablation of atrial fibrillation (AF) that provide optimal outcomes have remained controversial.ObjectivesWe evaluated the effects of left-atrial (LA) ablation of AF compared with bi-atrial (BA) ablation on the clinical and rhythm outcomes, and examined the predictors for AF recurrence and permanent pacing in consideration of ablation lesion sets.MethodsBetween 2001 and 2018, 1,965 patients underwent surgical ablation during cardiac surgery at our institution. Among these, 796 and 1,169 patients underwent LA and BA ablation, respectively. The clinical outcomes were evaluated after propensity score adjustment, with death accounting for a competing event. The probability of AF recurrence was estimated with the generalized estimating equations model.ResultsThe patients with BA ablation had morbidities greater than those with LA ablation. The probability of AF recurrence at 1 and 5 years was 13.9% and 37.1% in patients with LA ablation, and 11.2% and 30.1% in those with BA ablation (hazard ratio [HR]: 1.24; 95% confidence interval [CI]: 0.96-1.61; P = 0.100). After adjustment, LA ablation was associated with a decreased risk of early death (<30 days) (odds ratio [OR]: 0.56; 95% CI: 0.31-0.96; P = 0.041) and new-onset dialysis (OR 0.47; 95% CI: 0.27-0.78; P = 0.003). However, the risk of overall mortality (HR: 1.03; 95% CI: 0.75-1.41; P = 0.878) and permanent pacing (HR: 0.68; 95% CI: 0.43-1.06; P = 0.091) was comparable between the 2 groups.ConclusionsThe risk of AF recurrence and adverse events was comparable between the 2 ablation lesion sets. BA ablation was not related to an increased risk of permanent pacing.

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FOXM1D potentiates PKM2-mediated tumor glycolysis and angiogenesis.

Project description:Tumor growth, especially in the late stage, requires adequate nutrients and rich vasculature, in which PKM2 plays a convergent role. It has been reported that PKM2, together with FOXM1D, is upregulated in late-stage colorectal cancer and associated with metastasis; however, their underlying mechanism for promoting tumor progression remains elusive. Herein, we revealed that FOXM1D potentiates PKM2-mediated glycolysis and angiogenesis through multiple protein-protein interactions. In the presence of FBP, FOXM1D binds to tetrameric PKM2 and assembles a heterooctamer, restraining PKM2 metabolic activity by about a half and thereby promoting aerobic glycolysis. Furthermore, FOXM1D interacts with PKM2 and NF-κB and induces their nuclear translocation with the assistance of the nuclear transporter importin 4. Once in the nucleus, PKM2 and NF-κB complexes subsequently augment VEGFA transcription. The increased VEGFA is secreted extracellularly via exosomes, an event potentiated by the interaction of FOXM1 with VPS11, eventually promoting tumor angiogenesis. Based on these findings, our study provides another insight into the role of PKM2 in the regulation of glycolysis and angiogenesis.

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