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10.1002/advs.202510801 http://scihub22266oqcxt.onion/10.1002/advs.202510801 41355704!?!41355704 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41355704&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Adv+Sci+(Weinh) 2025 ; ? (?): e10801 Nephropedia Template TP {{tp|p=41355704|t=2025. ACSL5 Regulates Glucose Metabolism and Chemotherapy Sensitivity in Colorectal Cancer Cells under Glutamine Deficiency |pdf=|usr=}}{{41355704}} gab.com Text ACSL5 Regulates Glucose Metabolism and Chemotherapy Sensitivity in Colorectal Cancer Cells under Glutamine Deficiency JO: Adv Sci (Weinh) http://www.kidney.de/pget.php?&tw=1&pmid=41355704 #FOAvip Glutamine metabolism is crucial for sustaining tumor cell viability and growth, broadly promoting prospects for the therapeutic targeting of glutamine dependence. However, further research is needed to address key translational issues, particularly to better understand the adaptive survival responses employed by cancer cells in overcoming nutrient deficiency. Long-chain acyl-CoA synthetase 5 (ACSL5) is found to be upregulated under glutamine deprivation, acting to sustain tumor cell viability by enhancing both glycolytic flux and oxidative phosphorylation. ACSL5 operates within a p53 regulatory loop: p53 transcriptionally upregulates ACSL5, while ACSL5 competes with MIB1 to stabilize MDM2, suppressing p53 expression. Mechanistically, ACSL5 relieves p53-mediated inhibition of PGAM1 to drive glycolysis, while its mitochondrial localization promotes IDH2 activation to accelerate the TCA cycle. Nonetheless, these metabolic increases also generate reactive oxygen species (ROS), inducing DNA damage and significantly enhancing colorectal cancer cell sensitivity to oxaliplatin. The latter provides an explanation as to why colorectal tumors with high ACSL5 expression display preferentially improved patient outcomes from chemotherapy. Collectively, the findings reveal a new pathway for non-genetic chemotherapy resistance mechanisms, deepen the understanding of metabolic reprogramming in tumor cells, and offer potential therapeutic targets for future treatment strategies. Twit Text FOAVip ACSL5 Regulates Glucose Metabolism and Chemotherapy Sensitivity in Colorectal Cancer Cells under Glutamine Deficiency ????Adv Sci (Weinh) http://www.kidney.de/pget.php?&tw=1&pmid=41355704 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41355704 #FOAvip English Wikipedia <ref>{{Cite pmid|41355704}}</ref> ACSL5 Regulates Glucose Metabolism and Chemotherapy Sensitivity in Colorectal Cancer Cells under Glutamine Deficiency #MMPMID41355704 Tian S; Zhang Q; Sun X; Thorne RF; Shi Z; Ji Q; Sun Z; Lu Y; Zhao Q; Yu X; Hu W; Wu M Adv Sci (Weinh) 2025[Dec]; ? (?): e10801 PMID41355704show ga Glutamine metabolism is crucial for sustaining tumor cell viability and growth, broadly promoting prospects for the therapeutic targeting of glutamine dependence. However, further research is needed to address key translational issues, particularly to better understand the adaptive survival responses employed by cancer cells in overcoming nutrient deficiency. Long-chain acyl-CoA synthetase 5 (ACSL5) is found to be upregulated under glutamine deprivation, acting to sustain tumor cell viability by enhancing both glycolytic flux and oxidative phosphorylation. ACSL5 operates within a p53 regulatory loop: p53 transcriptionally upregulates ACSL5, while ACSL5 competes with MIB1 to stabilize MDM2, suppressing p53 expression. Mechanistically, ACSL5 relieves p53-mediated inhibition of PGAM1 to drive glycolysis, while its mitochondrial localization promotes IDH2 activation to accelerate the TCA cycle. Nonetheless, these metabolic increases also generate reactive oxygen species (ROS), inducing DNA damage and significantly enhancing colorectal cancer cell sensitivity to oxaliplatin. The latter provides an explanation as to why colorectal tumors with high ACSL5 expression display preferentially improved patient outcomes from chemotherapy. Collectively, the findings reveal a new pathway for non-genetic chemotherapy resistance mechanisms, deepen the understanding of metabolic reprogramming in tumor cells, and offer potential therapeutic targets for future treatment strategies. ?ACSL5 Regulates Glucose Metabolism and Chemotherapy Sensitivity in Col(epmc).pdf DeepDyve Pubget Overpricing