UHRF1 promotes aerobic glycolysis and proliferation via suppression of SIRT4 in pancreatic cancer

Hu, Qiangsheng; Qin, Yi; Ji, Shunrong; Xu, Wenyan; Liu, Wensheng; Sun, Qiqing; Zhang, Zheng; Liu, Mengqi; Ni, Quanxing; Lei, Yu; Xu, Xiaowu

doi:10.1016/j.canlet.2019.03.024

Cited by 116 publications

(81 citation statements)

References 51 publications

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“…Indeed, a variety of human cancers including lung, bladder, gastric, and breast cancers as well as leukemia have decreased SIRT4 expression and lower SIRT4 level was associated with poorer prognosis ( 46 , 47 ). Recently, SIRT4 has been demonstrated to inhibit PDAC cell proliferation and serves as a negative regulator of aerobic glycolysis in pancreatic cancer ( 48 ). Hence, whether SIRT4 exhibits tumor suppressive functions to negatively regulate glutamine metabolism by inhibiting GLUD in pancreatic cancer requires more research.…”

Section: Regulation Of the Reprogrammed Amino Acid Metabolism In Pdacmentioning

confidence: 99%

Reprogramming of Amino Acid Metabolism in Pancreatic Cancer: Recent Advances and Therapeutic Strategies

Yang

Ren

et al. 2020

Front. Oncol.

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies with an extremely poor prognosis. Energy metabolism reprogramming, an emerging hallmark of cancer, has been implicated in the tumorigenesis and development of pancreatic cancer. In addition to well-elaborated enhanced glycolysis, investigating the role of reprogramming of amino acid metabolism has sparked great interests in recent years. The rewiring amino acid metabolism orchestrated by genetic alterations contributes to pancreatic cancer malignant characteristics including cell proliferation, invasion, metastasis, angiogenesis and redox balance. In the unique hypoperfused and nutrient-deficient tumor microenvironment (TME), the interactions between cancer cells and stromal components and salvaging processes including autophagy and macropinocytosis play critical roles in fulfilling the metabolic requirements and supporting growth of PDAC. In this review, we elucidate the recent advances in the amino acid metabolism reprogramming in pancreatic cancer and the mechanisms of amino acid metabolism regulating PDAC progression, which will provide opportunities to develop promising therapeutic strategies.

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Section: Regulation Of the Reprogrammed Amino Acid Metabolism In Pdacmentioning

confidence: 99%

Reprogramming of Amino Acid Metabolism in Pancreatic Cancer: Recent Advances and Therapeutic Strategies

Yang

Ren

et al. 2020

Front. Oncol.

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“…There are reports that SIRT4 functions as a tumor suppressor, restraining the growth and proliferation of cells [56,[92][93][94]. SIRT4 can induce G1 cell cycle arrest by inhibiting phosphorylated extracellular signal-regulated kinase, cyclin D and cyclin E in gastric cancer [92].…”

Section: Tumorigenesismentioning

confidence: 99%

The Roles of Sirtuin Family Proteins in Cancer Progression

Zhao

Hou

et al. 2019

Cancers

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Sirtuin family members are characterized by either mono-ADP-ribosyltransferase or deacylase activity and are linked to various cancer-related biological pathways as regulators of transcriptional progression. Sirtuins play fundamental roles in carcinogenesis and maintenance of the malignant phenotype, mainly participating in cancer cell viability, apoptosis, metastasis, and tumorigenesis. Although sirtuin family members have a high degree of homology, they may play different roles in various kinds of cancer. This review highlights their fundamental roles in tumorigenesis and cancer development and provides a critical discussion of their dual roles in cancer, namely, as tumor promoters or tumor suppressors.

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“…In non-small cell lung cancer cell lines, SIRT4 reduced mitochondrial fission by interacting with the Fis-1/Drp1 axis and regulated cell invasive abilities by repressing MEK/ERK activity ( 81 ). A study also demonstrated that SIRT4 is a substrate of ubiquitin-like with plant homeodomain and ring finger domains 1 (UHRF1) and negatively regulated aerobic glycolysis, tumor proliferation, and metastasis of pancreatic cancer cells ( 95 ). A recent study also suggested that SIRT4 overexpression could heighten the sensitivity of ER-positive breast cancer to tamoxifen via inhibiting the interleukin-6/STAT3 pathway ( 102 ).…”

Section: Functions Of Sirt4 In Human Cancermentioning

confidence: 99%

Functions of mammalian SIRT4 in cellular metabolism and research progress in human cancer (Review)

et al. 2020

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Sirtuins are mammalian homologs of yeast silent information regulator two (SIRT) and are a highly conserved family of proteins, which act as nicotinamide adenine dinucleotide (NAD + )-dependent histone deacetylases. The seven sirtuins (SIRT1-7) share a conserved catalytic core domain; however, they have different enzyme activities, biological functions, and subcellular localizations. Among them, mitochondrial SIRT4 possesses ADP-ribosyltransferase, NAD + -dependent deacetylase, lipoamidase, and long-chain deacylase activities and can modulate the function of substrate proteins via ADP-ribosylation, delipoylation, deacetylation and long-chain deacylation. SIRT4 has been shown to play a crucial role in insulin secretion, fatty acid oxidation, amino acid metabolism, ATP homeostasis, apoptosis, neurodegeneration, and cardiovascular diseases. In addition, recent studies have demonstrated that SIRT4 acts as a tumor suppressor. Here, the present review summarizes the enzymatic activities and biological functions of SIRT4, as well as its roles in cellular metabolism and human cancer, which are described in the current literature.

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UHRF1 promotes aerobic glycolysis and proliferation via suppression of SIRT4 in pancreatic cancer

Cited by 116 publications

References 51 publications

Reprogramming of Amino Acid Metabolism in Pancreatic Cancer: Recent Advances and Therapeutic Strategies

Reprogramming of Amino Acid Metabolism in Pancreatic Cancer: Recent Advances and Therapeutic Strategies

The Roles of Sirtuin Family Proteins in Cancer Progression

Functions of mammalian SIRT4 in cellular metabolism and research progress in human cancer (Review)

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