2017
DOI: 10.1016/j.canlet.2016.09.020
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Acetyl-CoA carboxylase rewires cancer metabolism to allow cancer cells to survive inhibition of the Warburg effect by cetuximab

Abstract: Cetuximab inhibits HIF-1-regulated glycolysis in cancer cells, thereby reversing the Warburg effect and leading to inhibition of cancer cell metabolism. AMP-activated protein kinase (AMPK) is activated after cetuximab treatment, and a sustained AMPK activity is a mechanism contributing to cetuximab resistance. Here, we investigated how acetyl-CoA carboxylase (ACC), a downstream target of AMPK, rewires cancer metabolism in response to cetuximab treatment. We found that introduction of experimental ACC mutants l… Show more

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Cited by 69 publications
(47 citation statements)
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“…Western blot analysis was performed using the enhanced chemiluminescence detection kit (Amersham Biosciences) after incubation of the nitrocellulose membrane with various primary antibodies and horseradish peroxidase-labeled secondary antibodies [3941]. Immunoprecipitation was performed by subjecting cell lysates to reaction with respective primary antibodies and protein A sepharose beads (Amersham Biosciences) at 4°C overnight.…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…Western blot analysis was performed using the enhanced chemiluminescence detection kit (Amersham Biosciences) after incubation of the nitrocellulose membrane with various primary antibodies and horseradish peroxidase-labeled secondary antibodies [3941]. Immunoprecipitation was performed by subjecting cell lysates to reaction with respective primary antibodies and protein A sepharose beads (Amersham Biosciences) at 4°C overnight.…”
Section: Methodsmentioning
confidence: 99%
“…Hematoxylin was used for cell nuclear counterstaining. ImageJ image processing tool was used to quantify relative ASCT2 expression in cells after various treatments [4146]. …”
Section: Methodsmentioning
confidence: 99%
“…The finding about the contradictory roles of the ambiguous enzymes in promoting cell proliferation and suppressing the Warburg effect was also supported by several lines of literature-based evidence. For instance, the model-predicted ambiguous enzyme, acetyl-CoA carboxylase (ACC), was shown to shift cancer metabolism from glycolysis-dependent to lipogenesis-dependent in human head and neck squamous cell carcinoma (HNSCC) cells [47] and suppress whole-body glycolysis in high-fat-fed mice [48], while its inhibition impaired proliferation of human prostate cancer cells [49]. Another model-predicted ambiguous enzyme, proline dehydrogenase (PRODH/POX), was shown to suppress lactate production in human colon cancer cells [50], while its inhibition impaired proliferation of human lung cancer cells [51] and breast cancer cells [52].…”
Section: Metabolic Targets Identified By Pareto Surface Analysis Are mentioning
confidence: 99%
“…Short interfering RNA (siRNA) knockdown of ACC1 expression induced apo- ptosis in prostate (Brusselmans et al 2005) and breast (Chajes et al 2006) cancer cells and in cisplatin-resistant lung cancer cell lines (Wangpaichitr et al 2012), and chemical inhibition of ACC1 and ACC2 by the macrocyclic myxobacterial natural product Soraphen A led to growth arrest in breast cancer cells (Beckers et al 2007) and induction of apoptosis in prostate cancer cells (Corominas-Faja et al 2014). Constitutively active ACC mutants also protected head and neck squamous cancer cells from cetuximab-induced growth inhibition (Luo et al 2016). However, although these observations provide compelling data that ACC mediates cellular proliferation, these studies were exclusively in vitro and did not address whether ACC activation was required for tumor growth in vivo, as the genetic role of ACC in tumor growth had not been investigated.…”
Section: Acc As An Anticancer Drug Targetmentioning
confidence: 99%