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Glutamine, as the most abundant amino acid in the body, participates in the biological synthesis of nucleotides and other non-essential amino acids in the process of cell metabolism. Recent studies showed that glutamine metabolic reprogramming is an important signal during cancer development and progression. This metabolic signature in cancer cells can promote the development of cancer by activating multiple signaling pathways and oncogenes. It can also be involved in tumor immune regulation and promote the development of drug resistance to tumors. In this review, we mainly summarize the role of glutamine metabolic reprogramming in tumors, including the regulation of multiple signaling pathways. We further discussed the promising tumor treatment strategy by targeting glutamine metabolism alone or in combination with chemotherapeutics.
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Glutamina , Neoplasias , Humanos , Glutamina/metabolismo , Neoplasias/patología , Transformación Celular Neoplásica/metabolismo , Aminoácidos , Resistencia a Múltiples MedicamentosRESUMEN
Galectin-4, a tandem repeat member of the β-galactoside-binding proteins, possesses two carbohydrate-recognition domains (CRD) in a single peptide chain. This lectin is mostly expressed in epithelial cells of the intestinal tract and secreted to the extracellular. The two domains have 40% similarity in amino acid sequence, but distinctly binding to various ligands. Just because the two domains bind to different ligands simultaneously, galectin-4 can be a crosslinker and crucial regulator in a large number of biological processes. Recent evidence shows that galectin-4 plays an important role in lipid raft stabilization, protein apical trafficking, cell adhesion, wound healing, intestinal inflammation, tumor progression, etc. This article reviews the physiological and pathological features of galectin-4 and its important role in such processes.
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Animales , Humanos , Axones , Metabolismo , Endocitosis , Galectina 4 , Sangre , Genética , Metabolismo , Enfermedades Inflamatorias del Intestino , Metabolismo , Patología , Microdominios de Membrana , Metabolismo , Neoplasias , Metabolismo , Patología , Neuronas , Metabolismo , Cicatrización de HeridasRESUMEN
Objective: To discuss the effect of BRMS1 on the proliferation, migration and adhesion of mouse forestomach carcinoma. Methods: The constructed pCMV-myc- BRMS1 recombinant plasmid and blank plasmid were transfected into mouse forestomach carcinoma. MTT method was employed to measure the activity of gastric cancer cell; the scratch assay and Transwell assay to measure the migration and invasion of gastric cancer cell; the adhesion assay to measure the adhesion of gastric cancer cell; while the Western blot assay to measure the expression of The NF-κB signal pathway, downstream matrix metalloproteinase (MMP)-2, MMP-9 and osteopontin and E-cadherin in the gastric cancer cell. Besides, the transplanted animal model of gastric cancer in mice was constructed to measure the size of tumor xenograft. Results: Results of MTT assay showed that, compared with the empty vector control group, the activity of gastric cancer cell was not affected in the BRMS1 transfection group. The improved expression of BRMS1 could inhibit the adhesion, migration and invasion of gastric cancer cell (P < 0.01). Besides, compared with the empty vector control group, the phosphorylation of NF-κB p65 and IκBα was reduced in the BRMS1 transfection group, with the decreased expression of MMP-2, MMP-9 and osteopontin and the increased expression of E-cadherin (P < 0.01). Results of animal experiment also showed that the expression of BRMS1 did not affect the transplanted tumor. Conclusions: The expression of BRMS1 can significantly inhibit the adhesion, migration, invasion and metastasis of mouse forestomach carcinoma gastric cancer cell, which is related to The NF-κB signal pathway.
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OBJECTIVE@#To discuss the effect of BRMS1 on the proliferation, migration and adhesion of mouse forestomach carcinoma.@*METHODS@#The constructed pCMV-myc-BRMS1 recombinant plasmid and blank plasmid were transfected into mouse forestomach carcinoma. MTT method was employed to measure the activity of gastric cancer cell; the scratch assay and Transwell assay to measure the migration and invasion of gastric cancer cell; the adhesion assay to measure the adhesion of gastric cancer cell; while the Western blot assay to measure the expression of The NF-κB signal pathway, downstream matrix metalloproteinase (MMP)-2, MMP-9 and osteopontin and E-cadherin in the gastric cancer cell. Besides, the transplanted animal model of gastric cancer in mice was constructed to measure the size of tumor xenograft.@*RESULTS@#Results of MTT assay showed that, compared with the empty vector control group, the activity of gastric cancer cell was not affected in the BRMS1 transfection group. The improved expression of BRMS1 could inhibit the adhesion, migration and invasion of gastric cancer cell (P < 0.01). Besides, compared with the empty vector control group, the phosphorylation of NF-κB p65 and IκBα was reduced in the BRMS1 transfection group, with the decreased expression of MMP-2, MMP-9 and osteopontin and the increased expression of E-cadherin (P < 0.01). Results of animal experiment also showed that the expression of BRMS1 did not affect the transplanted tumor.@*CONCLUSIONS@#The expression of BRMS1 can significantly inhibit the adhesion, migration, invasion and metastasis of mouse forestomach carcinoma gastric cancer cell, which is related to The NF-κB signal pathway.
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Objective To investigate the effect ofYindanxinnaotong (YDXNT) capsule on learning and memory abilities, super oxide dismutase (SOD) activity and malondialdehyde (MDA) content in the hippocampus of rat models of vascular dementia (VD). Methods Animals were randomly divided into sham-operated group,VD vehicle group (Group VD) and YDXNT treatment group (Group VD+YDXNT); the 4-vessel occlusion was employed to establish the VD rat models in the Group VD and Group VD+YDXNT,while rats in the sham-operated group were not performed occlusion of the bilateral common carotid artery.Rats of the Group VD+YDXNT were given 1 mL liquid (9 granules of YDXNT into 360 mL normal saline) through intragastric administration 3 times daily for a consecutive 4 weeks; and rats of the other 2 groups were given the same volume of saline.The changes of learning and memory abilities were observed by Morris water maze test; the activity of SOD and the content of MDA in the hippocampus were measured. Results As compared with those in rats of the Group VD, the learning and memory abilities in rats of the Group VD+YDXNT were significantly improved (P<0.05):time in finding the platform was obviously decreased and swimming distance in finding the platform was obviously shortened in rats of Group VD+YDXNT.As compared with those in rats of the Group VD,the activity of SOD in the hippocampus was significantly increased and the content of MDA was obviously decreased in rats of the Group VD+YDXNT (P<0.05). Conclusion YDXNT could increase oxygen radical metabolism to improve the learning and memory abilities of rats with VD.
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Objective To study the effect of Yindan Xinnaotong Capsules (YDXNT) on impairment of learning and memory in rats with vascular dementia (VD) and acetylcholinesterase (AchE) level of the hippocampus,and observe the mechanism of YDXNT in VD. Methods Bilateral carotid arteries were repeatedly blocked and performed reperfusion with nitroprusside sodium by intraperitoneal injection to establish the rat models of VD.VD rat models were randomly divided into VD model group (n=10) and YDXNT treatment group (n=10),and another 10 condition-matched rats were selected as the sham-operated group.At 30 min after regaining consciousness and before execution,the neurological scale was performed on these rats; the effect of YDXNT on learning and memory in rats were tested by step-down avoidance tests; rats' brains were dissected out on the ice for detecting the activity of AchE.Results The scores of neurological scale in the YDXNT treatment group and VD model group were obviously higher than those in the sham-operated group (P<0.05); the scores of neurological scale in the YDXNT treatment group were significantly lower than those in the VD model group (P<0.05).In the step-down avoidance tests,the rats in the YDXNT treatment group had significantly shorter reaction time,less number of errors and longer latency than rats in the VD model group (P<0.05).As compared with that in the VD model group,the activity of AChE in the hippocampus of YDXNT treatment group was significantly decreased (P<0.05). Conclnsion YDXNT can ameliorate the learning and memory deficits of VD model rats and the mechanism may be its involvement in inhibiting the AChE activity.