Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma

An, Fangyu; Chang, Weirong; Song, Jiayi; Zhang, Jie; Li, Zhonghong; Gao, Peng; Wang, Yujie; Xiao, Zhipan; Yan, Chunlu

doi:10.1016/j.jbo.2024.100521

Cited by 2 publications

(2 citation statements)

References 145 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Energy metabolism is the process of releasing energy after nutrients in the organism are catalyzed by various enzymes. Glucose metabolism is one of the pathways of energy metabolism in aquatic animals, among which glycolysis is an important link of glucose metabolism that decomposes glucose or glycogen to keep the energy provision of the body [35,36]. PDH, HK, and PK are key rate-limiting enzymes in glycolysis, and LDH is an important coenzyme in glucose metabolism [14,37].…”

Section: Discussionmentioning

confidence: 99%

Toxicity of Ammonia Stress on the Physiological Homeostasis in the Gills of Litopenaeus vannamei under Seawater and Low-Salinity Conditions

Nan,

Xiao,

Duan

et al. 2024

Biology

View full text Add to dashboard Cite

Ammonia is a major water quality factor influencing the survival and health of shrimp, among which the gill is the main effector organ for ammonia toxicity. In this study, we chose two types of Litopenaeus vannamei that were cultured in 30‰ seawater and domesticated in 3‰ low salinity, respectively, and then separately subjected to ammonia stress for 14 days under seawater and low-salinity conditions, of which the 3‰ low salinity-cultured shrimp were domesticated from the shrimp cultured in 30‰ seawater after 27 days of gradual salinity desalination. In detail, this study included four groups, namely the SC group (ammonia-N 0 mg/L, salinity 30‰), SAN group (ammonia-N 10 mg/L, salinity 30‰), LC group (ammonia-N 0 mg/L, salinity 3‰), and LAN group (ammonia-N 10 mg/L, salinity 3‰). The ammonia stress lasted for 14 days, and then the changes in the morphological structure and physiological function of the gills were explored. The results show that ammonia stress caused the severe contraction of gill filaments and the deformation or even rupture of gill vessels. Biochemical indicators of oxidative stress, including LPO and MDA contents, as well as T-AOC and GST activities, were increased in the SAN and LAN groups, while the activities of CAT and POD and the mRNA expression levels of antioxidant-related genes (nrf2, cat, gpx, hsp70, and trx) were decreased. In addition, the mRNA expression levels of the genes involved in ER stress (ire1 and xbp1), apoptosis (casp-3, casp-9, and jnk), detoxification (gst, ugt, and sult), glucose metabolism (pdh, hk, pk, and ldh), and the tricarboxylic acid cycle (mdh, cs, idh, and odh) were decreased in the SAN and LAN groups; the levels of electron-transport chain-related genes (ndh, cco, and coi), and the bip and sdh genes were decreased in the SAN group but increased in the LAN group; and the level of the ATPase gene was decreased but the cytc gene was increased in the SAN and LAN groups. The mRNA expression levels of osmotic regulation-related genes (nka-β, ca, aqp and clc) were decreased in the SAN group, while the level of the ca gene was increased in the LAN group; the nka-α gene was decreased in both two groups. The results demonstrate that ammonia stress could influence the physiological homeostasis of the shrimp gills, possibly by damaging the tissue morphology, and affecting the redox, ER function, apoptosis, detoxification, energy metabolism, and osmoregulation.

show abstract

Section: Discussionmentioning

confidence: 99%

Toxicity of Ammonia Stress on the Physiological Homeostasis in the Gills of Litopenaeus vannamei under Seawater and Low-Salinity Conditions

Nan,

Xiao,

Duan

et al. 2024

Biology

View full text Add to dashboard Cite

show abstract

“…Next, we investigated whether CoQ 0 modulated metabolic reprogramming and the Warburg effect in HNSCC cells. HIF-1α activation regulates critical enzymes that are associated with aerobic glycolysis, which alternately feed into the Warburg effect 58 . We found that CoQ 0 decreased glucose absorption and L-lactate accumulation in OECM-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Yang,

Chang,

Vadivalagan

et al. 2024

Int. J. Biol. Sci.

View full text Add to dashboard Cite

Coenzyme Q0 (CoQ0), a quinone derivative from Antrodia camphorata, has antitumor capabilities. This study investigated the antitumor effect of noncytotoxic CoQ0, which included NLRP3 inflammasome inhibition, anti-EMT/metastasis, and metabolic reprogramming via HIF-1α inhibition, in HNSCC cells under normoxia and hypoxia. CoQ0 suppressed hypoxia-induced ROS-mediated HIF-1α expression in OECM-1 and SAS cells. Under normoxia and hypoxia, the inflammatory NLRP3, ASC/caspase-1, NFκB, and IL-1β expression was reduced by CoQ0. CoQ0 reduced migration/invasion by enhancing epithelial marker E-cadherin and suppressing mesenchymal markers Twist, N-cadherin, Snail, and MMP-9, and MMP-2 expression. CoQ0 inhibited glucose uptake, lactate accumulation, GLUT1 levels, and HIF-1α−target gene (HK-2, PFK-1, and LDH-A) expressions that are involved in aerobic glycolysis. Notably, CoQ0 reduced ECAR as well as glycolysis, glycolytic capability, and glycolytic reserve and enhanced OCR, basal respiration, ATP generation, maximal respiration, and spare capacity in OECM-1 cells. Metabolomic analysis using LC-ESI-MS showed that CoQ0 treatment decreased the levels of glycolytic intermediates, including lactate, 2/3-phosphoglycerate, fructose 1,6-bisphosphate, and phosphoenolpyruvate, and increased the levels of TCA cycle metabolites, including citrate, isocitrate, and succinate. HIF-1α silencing reversed CoQ0-mediated anti-metastasis (N-Cadherin, Snail, and MMP-9) and metabolic reprogramming (GLUT1, HK-2, and PKM-2) under hypoxia. CoQ0 prevents cancer stem-like characteristics (upregulated CD24 expression and downregulated CD44, ALDH1, and OCT4) under normoxia and/or hypoxia. Further, in IL-6-treated SG cells, CoQ0 attenuated fibrosis by inhibiting TGF-β and Collagen I expression and suppressed EMT by downregulating Slug and upregulating E-cadherin expression. Interesting, CoQ0 inhibited the growth of OECM-1 tumors in xenografted mice. Our results advocate CoQ0 for the therapeutic application against HNSCC.

show abstract

Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma

Cited by 2 publications

References 145 publications

Toxicity of Ammonia Stress on the Physiological Homeostasis in the Gills of Litopenaeus vannamei under Seawater and Low-Salinity Conditions

Toxicity of Ammonia Stress on the Physiological Homeostasis in the Gills of Litopenaeus vannamei under Seawater and Low-Salinity Conditions

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Contact Info

Product

Resources

About

Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma

Cited by 2 publications

References 145 publications

Toxicity of Ammonia Stress on the Physiological Homeostasis in the Gills of Litopenaeus vannamei under Seawater and Low-Salinity Conditions

Toxicity of Ammonia Stress on the Physiological Homeostasis in the Gills of Litopenaeus vannamei under Seawater and Low-Salinity Conditions

Coenzyme Q0 inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells

Contact Info

Product

Resources

About

Coenzyme Q₀ inhibited the NLRP3 inflammasome, metastasis/EMT, and Warburg effect by suppressing hypoxia-induced HIF-1α expression in HNSCC cells