Reprogramming of glycolysis by chemical carcinogens during tumor development

D’Souza, Leonard Clinton; Shekher, Anusmita; Challagundla, Kishore B.; Sharma, Anurag; Gupta, Subash C.

doi:10.1016/j.semcancer.2022.10.004

Cited by 13 publications

(6 citation statements)

References 117 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The DNA MMR system recognizes and corrects occasional DNA base mismatches in non-homologous chromosomes during DNA replication, and this correction ensures the stability and integrity of the genome ( 39 ). Deficiencies in the MMR system can lead to genetic mutations and induce tumorigenesis ( 40 ).…”

Section: Discussionmentioning

confidence: 99%

Role of prognostic gene DKK1 in oral squamous cell carcinoma

Liu,

Wei,

Wang

et al. 2023

Oncol Lett

View full text Add to dashboard Cite

Oral squamous cell carcinoma (OSCC) is one of the most common squamous cell carcinomas of the head and neck. The morbidity and mortality rates of OSCC have increased in recent years. However, the pathogenesis of this disease remains unknown. The present study aimed to identify predictive biomarkers and therapeutic targets for OSCC. Bioinformatics screening of differentially expressed genes in OSCC was performed based on data from The Cancer Genome Atlas and Gene Expression Omnibus databases. Dickkopf Wnt signaling pathway inhibitor 1 (DKK1) was identified to be associated with survival, tumor immunity and DNA repair in OSCC. Furthermore, the effects of DKK1 were evaluated by the knockdown of DKK1 in two OSCC cell lines. The proliferation, clonogenicity, migration and invasion of the cells were assessed in vitro using Cell Counting Kit-8, colony formation, wound healing and Transwell assays, respectively, and were found to be inhibited by DKK1 knockdown. The present study suggests that DKK1 may be used in the prognosis of patients with OSCC and that targeting DKK1 is a potential strategy for OSCC therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Role of prognostic gene DKK1 in oral squamous cell carcinoma

Liu,

Wei,

Wang

et al. 2023

Oncol Lett

View full text Add to dashboard Cite

show abstract

“…Emerging evidence has revealed that alterations in HIF‐1α, oncogenes, and tumor suppressor genes lead to upregulated expression of GLUTs and key metabolic enzymes of glucose metabolism, thereby increasing the rate of glucose metabolism in various cancer types, including lung, breast, liver, and oral cancer 254,255 . For example, MYC, the major regulator of cell growth, enhances the expression of diverse transporters and enzymes during glycolysis, including GLUT1, hexokinase 2 (HK2), pyruvate dehydrogenase kinase isozyme 1 (PDK1), and lactate dehydrogenase A (LDHA) 256–258 . The tumor suppressor p53, which holds prominence, has also been demonstrated to upregulate the glycolytic pathway and disrupt the equilibrium between anabolism and redox interactions 259 .…”

Section: Rna Methylation and Cancer Metabolismmentioning

confidence: 99%

“… 254 , 255 For example, MYC, the major regulator of cell growth, enhances the expression of diverse transporters and enzymes during glycolysis, including GLUT1, hexokinase 2 (HK2), pyruvate dehydrogenase kinase isozyme 1 (PDK1), and lactate dehydrogenase A (LDHA). 256 , 257 , 258 The tumor suppressor p53, which holds prominence, has also been demonstrated to upregulate the glycolytic pathway and disrupt the equilibrium between anabolism and redox interactions. 259 It is generally acknowledged that glucose transport across the plasma membrane, facilitated by GLUTs, is the first rate‐limiting stage in glucose utilization.…”

Section: Rna Methylation and Cancer Metabolismmentioning

confidence: 99%

Critical roles and clinical perspectives of RNA methylation in cancer

Li,

Yao,

Liu

et al. 2024

MedComm

View full text Add to dashboard Cite

RNA modification, especially RNA methylation, is a critical posttranscriptional process influencing cellular functions and disease progression, accounting for over 60% of all RNA modifications. It plays a significant role in RNA metabolism, affecting RNA processing, stability, and translation, thereby modulating gene expression and cell functions essential for proliferation, survival, and metastasis. Increasing studies have revealed the disruption in RNA metabolism mediated by RNA methylation has been implicated in various aspects of cancer progression, particularly in metabolic reprogramming and immunity. This disruption of RNA methylation has profound implications for tumor growth, metastasis, and therapy response. Herein, we elucidate the fundamental characteristics of RNA methylation and their impact on RNA metabolism and gene expression. We highlight the intricate relationship between RNA methylation, cancer metabolic reprogramming, and immunity, using the well‐characterized phenomenon of cancer metabolic reprogramming as a framework to discuss RNA methylation's specific roles and mechanisms in cancer progression. Furthermore, we explore the potential of targeting RNA methylation regulators as a novel approach for cancer therapy. By underscoring the complex mechanisms by which RNA methylation contributes to cancer progression, this review provides a foundation for developing new prognostic markers and therapeutic strategies aimed at modulating RNA methylation in cancer treatment.

show abstract

“…Thus, early detection of abnormal esophageal epithelial cells is crucial for diagnosing and treating EC, such as Barrett's esophagus, 5 esophageal epithelial cells dysplasia, 6 glycolysis deregulation, 7 and other premalignant conditions. Glucose metabolism reprogramming is a prerequisite for tumorigenesis 8,9 . Under normoxic conditions, cells metabolize glucose by aerobic glycolysis instead of oxidative phosphorylation to meet abnormal cell proliferation, growth, and survival, a phenomenon known as the “Warburg effect.” 9,10 Aerobic glycolysis is modulated by various oncogenes and glycolytic enzymes.…”

Section: Introductionmentioning

confidence: 99%

“…Glucose metabolism reprogramming is a prerequisite for tumorigenesis. 8,9 Under normoxic conditions, cells metabolize glucose by aerobic glycolysis instead of oxidative phosphorylation to meet abnormal cell proliferation, growth, and survival, a phenomenon known as the "Warburg effect." 9,10 Aerobic glycolysis is modulated by various oncogenes and glycolytic enzymes.…”

mentioning

confidence: 99%

Arecoline promotes Akt‐c‐Myc‐driven aerobic glycolysis in esophageal epithelial cells

Han,

Chen,

Huang

et al. 2024

Environmental Toxicology

View full text Add to dashboard Cite

Aerobic glycolysis is a typical metabolic rearrangement for tumorigenesis. Arecoline is of explicit carcinogenicity, numerous works demonstrate its mutagenicity, genotoxicity, and cytotoxicity. However, the effects of arecoline on aerobic glycolysis of esophageal epithelial cells remain unclear. In the present study, 5 μM arecoline efficiently increased HK2 expression to induce aerobic glycolysis in Het‐1A‐Are and NE2‐Are cells. The mechanistic analysis showed that arecoline activated the Akt‐c‐Myc signaling pathway and reduced the GSK3β‐mediated phosphorylation of c‐Myc on Thr58 to prevent its ubiquitination and destruction, subsequently promoting HK2 transcription and expression. Taken together, these results suggest that arecoline can induce aerobic glycolysis of esophageal epithelial cells and further confirm that arecoline is a carcinogen harmful to human health.

show abstract

Reprogramming of glycolysis by chemical carcinogens during tumor development

Cited by 13 publications

References 117 publications

Role of prognostic gene DKK1 in oral squamous cell carcinoma

Role of prognostic gene DKK1 in oral squamous cell carcinoma

Critical roles and clinical perspectives of RNA methylation in cancer

Arecoline promotes Akt‐c‐Myc‐driven aerobic glycolysis in esophageal epithelial cells

Contact Info

Product

Resources

About