S100A11 activates the pentose phosphate pathway to induce malignant biological behaviour of pancreatic ductal adenocarcinoma

Zeng, Xue; Guo, Hong; Liu, Zhuang; Qin, Zilan; Cong, Yuyang; Ren, Naihan; Zhang, Yuxiang; Zhang, Na

doi:10.1038/s41419-022-05004-3

Cited by 9 publications

(4 citation statements)

References 62 publications

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“…The inhibition of glucose 6-phosphate dehydrogenase (G6PD) has been shown to reduce omental metastasis of ovarian cancer cells, thus suggesting a role of PPP in peritoneal metastasis of ovarian cancers [51,52]. A similar role of PPP pathway intermediates has been observed in peritoneal metastasis involving gastric, pancreatic, and colorectal cancers [49,53,54]. It has also been observed that the key enzymes of PPP such as G6PD, transaldolase, and transketolase are upregulated in pleural mesothelioma cell lines, which has a certain degree of similarity with the peritoneal mesothelioma [55].…”

Section: Glucose Metabolismmentioning

confidence: 99%

Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies

Nadhan

Kashyap

et al. 2023

Metabolites

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Peritoneal cancers present significant clinical challenges with poor prognosis. Understanding the role of cancer cell metabolism and cancer-promoting metabolites in peritoneal cancers can provide new insights into the mechanisms that drive tumor progression and can identify novel therapeutic targets and biomarkers for early detection, prognosis, and treatment response. Cancer cells dynamically reprogram their metabolism to facilitate tumor growth and overcome metabolic stress, with cancer-promoting metabolites such as kynurenines, lactate, and sphingosine-1-phosphate promoting cell proliferation, angiogenesis, and immune evasion. Targeting cancer-promoting metabolites could also lead to the development of effective combinatorial and adjuvant therapies involving metabolic inhibitors for the treatment of peritoneal cancers. With the observed metabolomic heterogeneity in cancer patients, defining peritoneal cancer metabolome and cancer-promoting metabolites holds great promise for improving outcomes for patients with peritoneal tumors and advancing the field of precision cancer medicine. This review provides an overview of the metabolic signatures of peritoneal cancer cells, explores the role of cancer-promoting metabolites as potential therapeutic targets, and discusses the implications for advancing precision cancer medicine in peritoneal cancers.

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Section: Glucose Metabolismmentioning

confidence: 99%

Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies

Nadhan

Kashyap

et al. 2023

Metabolites

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“…Increased expression of the calcium-binding protein S100A11 in PDAC promotes the loading of H3K4me3 onto the TKT promoter, enhancing the PPP by increasing TKT levels and leading to worse clinical prognosis and disease progression. This suggests that S100A11 may be a possible therapeutic target ( Zeng et al, 2022 ). PPP is a branch of glycolysis.…”

Section: Alterations In Glucose Metabolismmentioning

confidence: 99%

The role of metabolic reprogramming in pancreatic cancer chemoresistance

Liu

2023

Front. Pharmacol.

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Pancreatic cancer is characterized by hidden onset, high malignancy, and early metastasis. Although a few cases meet the surgical indications, chemotherapy remains the primary treatment, and the resulting chemoresistance has become an urgent clinical problem that needs to be solved. In recent years, the importance of metabolic reprogramming as one of the hallmarks of cancers in tumorigenesis has been validated. Metabolic reprogramming involves glucose, lipid, and amino acid metabolism and interacts with oncogenes to affect the expression of key enzymes and signaling pathways, modifying the tumor microenvironment and contributing to the occurrence of drug tolerance. Meanwhile, the mitochondria are hubs of the three major nutrients and energy metabolisms, which are also involved in the development of drug resistance. In this review, we summarized the characteristic changes in metabolism during the progression of pancreatic cancer and their impact on chemoresistance, outlined the role of the mitochondria, and summarized current studies on metabolic inhibitors.

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“…S100A11 is a member of the S100 protein family and has high homology with calmodulin and EF-hand calcium-binding proteins, which promotes tumor progression through cell proliferation, metastasis, angiogenesis and immune evasion. Recent studies reported that S100A11 was an oncogene in pancreatic ductal adenocarcinoma [1,2], glioma [3][4][5], colorectal cancer [6], breast cancer [7], lung cancer [8], thyroid cancer [9], and gastric cancer [10]. However, the biological function of S100A11 in the tumor microenvironment (TME) has been rarely reported.…”

Section: Introductionmentioning

confidence: 99%

S100A11: A Potential Carcinogen and Prognostic Marker That Correlates with the Immunosuppressive Microenvironment in Pan-Cancer

Ji¹,

Qin²,

Huang³

et al. 2023

J. Cancer

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S100 calcium-binding protein A11 (S100A11) has been proved to be an oncogene of most tumors. However, its role in the tumor microenvironment (TME) in pan-cancer stills remains poorly understood. This study used public data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) database to evaluate the expression of S100A11. The R package “GSVA” was used for Gene set variation analysis (GSVA) of S100A11. The R package “ESTIMATE” was used to further explore the relationship between S100A11 and TME. The Genomics of Drug Sensitivity in Cancer database was used to investigate the effect of S100A11 on the efficiency of anticancer drugs. We found S100A11 expression was upregulated in most tumors and predicted a poor prognosis. Furthermore, S100A11 expression was closely associated with immune regulation-related pathways. Moreover, S100A11 expression in pan-cancer was significantly related to most immunosuppressive cells, such as tumor-associated macrophages (TAM), tumor-associated fibroblasts (TAF), and Treg cells. The expression of S100A11 was significantly related to immunosuppressive genes and immune checkpoints in most tumor types. Additionally, the upregulation of S100A11 expression made patients with cancer resistant to the treatment of most anticancer drugs, such as sorafenib. In brief, our study showed that S100A11 could be used as a potential carcinogen and prognostic marker for most tumor types. The increased expression of S100A11 was closely related to tumor immunosuppressive TME. The upregulation of S100A11 expression made patients with cancer resistant to sorafenib treatment.

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S100A11 activates the pentose phosphate pathway to induce malignant biological behaviour of pancreatic ductal adenocarcinoma

Cited by 9 publications

References 62 publications

Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies

Targeting Oncometabolites in Peritoneal Cancers: Preclinical Insights and Therapeutic Strategies

The role of metabolic reprogramming in pancreatic cancer chemoresistance

S100A11: A Potential Carcinogen and Prognostic Marker That Correlates with the Immunosuppressive Microenvironment in Pan-Cancer

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