2018
DOI: 10.18632/oncotarget.24676
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Glycogen debranching enzyme (AGL) is a novel regulator of non-small cell lung cancer growth

Abstract: Glycogen debranching enzyme (AGL) and Glycogen phosphorylase (PYG) are responsible for glycogen breakdown. We have earlier shown that AGL is a regulator of bladder tumor growth. Here we investigate the role of AGL in non-small cell lung cancers (NSCLC). Short hairpin RNA (shRNA) driven knockdown of AGL resulted in increased anchorage independent and xenograft growth of NSCLC cells. We further establish that an increase in hyaluronic acid (HA) synthesis driven by Hyaluronic Acid Synthase 2 (HAS2) is critical fo… Show more

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Cited by 12 publications
(10 citation statements)
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“…Low expression of enriched genes such as CYP2C19 [Ashida et al 2018], ABAT (4-aminobutyrate aminotransferase) [Jansen et al 2015], ACOX1 [Chen et al 2018], ACSM3 [Ruan et al 2017], FBP1 [Liu et al 2018], ST3GAL6 [Souady et al 2011], AGXT (alanine--glyoxylate and serine-- pyruvate aminotransferase) [Sun et al 2019], ALDOB (aldolase, fructose-bisphosphate B) [Tao et al 2015], ALDH6A1 [Shin et al 2020], XDH (xanthine dehydrogenase) [Chen et al 2017], OGDHL (oxoglutarate dehydrogenase like) [Jiao et al 2019], CYP2C8 [Li et al 2019], CYP2C9 [Yu et al 2015], CYP3A5 [Jiang et al 2015], BHMT (betaine--homocysteine S-methyltransferase) [Jin et al 2016], TAT (tyrosine aminotransferase) [Fu et al 2010], SLC27A5 [Gao et al 2020], GYS2 [Chen et al 2019], GLYAT (glycine-N-acyltransferase) [Matsuo et al 2012], CES3 [Quiroga et al 2016], MASP2 [Ding et al 2014], C7 [Seol et al 2016] and F11 [Du et al 2019] were involved in progression of hepatocellular carcinoma, but decrease expression these genes may be identified with growth of hepatoblastoma. Enriched genes such as SULT1A2 [Fernandez-Santander et al 2013], PIK3C2G [Li et al 2015], AGL (amylo-alpha-1, 6-glucosidase, 4-alpha-glucanotransferase) [Richmond et al 2018], UGT2B10 [Lu et al 2018], CTH (cystathionine gamma-lyase) [Xu et al 2020] and CYP26A1 [Osanai and Lee, 2015] were involved in metabolic activity of various cancer types, but these genes may liable for metabolic activity of in hepatoblastoma. Enriched genes such as TDO2 [Pham et al 2018], EPHX2 [Vainio et al 2011], PLA2G2A [Ganesan et al 2008], INPP1 [Li et al 2019], GCH1 [Gao et al 2016], GNE (glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase) [Kemmner et al 2012], PAPSS2 [Zhang et al 2019], GLYATL1 [Eich et al 2019], CFB (complement factor B) [Kim et al 2019], C1R [Riihilä et al 2020], C1S [Riihilä et al 2020], C9 [Chong et al 2010], FGB (fibrinogen beta chain) [Repetto et al 2018] and KNG1 [Quesada-Calvo et al 2017] were linked with development of various cancer types, but these genes may be culpable for advancement of hepatoblastoma.…”
Section: Discussionmentioning
confidence: 99%
“…Low expression of enriched genes such as CYP2C19 [Ashida et al 2018], ABAT (4-aminobutyrate aminotransferase) [Jansen et al 2015], ACOX1 [Chen et al 2018], ACSM3 [Ruan et al 2017], FBP1 [Liu et al 2018], ST3GAL6 [Souady et al 2011], AGXT (alanine--glyoxylate and serine-- pyruvate aminotransferase) [Sun et al 2019], ALDOB (aldolase, fructose-bisphosphate B) [Tao et al 2015], ALDH6A1 [Shin et al 2020], XDH (xanthine dehydrogenase) [Chen et al 2017], OGDHL (oxoglutarate dehydrogenase like) [Jiao et al 2019], CYP2C8 [Li et al 2019], CYP2C9 [Yu et al 2015], CYP3A5 [Jiang et al 2015], BHMT (betaine--homocysteine S-methyltransferase) [Jin et al 2016], TAT (tyrosine aminotransferase) [Fu et al 2010], SLC27A5 [Gao et al 2020], GYS2 [Chen et al 2019], GLYAT (glycine-N-acyltransferase) [Matsuo et al 2012], CES3 [Quiroga et al 2016], MASP2 [Ding et al 2014], C7 [Seol et al 2016] and F11 [Du et al 2019] were involved in progression of hepatocellular carcinoma, but decrease expression these genes may be identified with growth of hepatoblastoma. Enriched genes such as SULT1A2 [Fernandez-Santander et al 2013], PIK3C2G [Li et al 2015], AGL (amylo-alpha-1, 6-glucosidase, 4-alpha-glucanotransferase) [Richmond et al 2018], UGT2B10 [Lu et al 2018], CTH (cystathionine gamma-lyase) [Xu et al 2020] and CYP26A1 [Osanai and Lee, 2015] were involved in metabolic activity of various cancer types, but these genes may liable for metabolic activity of in hepatoblastoma. Enriched genes such as TDO2 [Pham et al 2018], EPHX2 [Vainio et al 2011], PLA2G2A [Ganesan et al 2008], INPP1 [Li et al 2019], GCH1 [Gao et al 2016], GNE (glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase) [Kemmner et al 2012], PAPSS2 [Zhang et al 2019], GLYATL1 [Eich et al 2019], CFB (complement factor B) [Kim et al 2019], C1R [Riihilä et al 2020], C1S [Riihilä et al 2020], C9 [Chong et al 2010], FGB (fibrinogen beta chain) [Repetto et al 2018] and KNG1 [Quesada-Calvo et al 2017] were linked with development of various cancer types, but these genes may be culpable for advancement of hepatoblastoma.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, other enzymes involved in glycogenolysis are thought to have tumor-suppressive roles. This includes the glycogen debranching enzyme AGL which had a suppressing function in models of bladder and lung cancers, and the kinase PhK β-subunit (PHKB) which suppressed models of hepatocellular carcinoma (18)(19)(20)(21). Interestingly, these tumor suppressive roles are potentially independent of glycogen metabolism (19,21).…”
Section: Reprogrammed Glycogen Metabolism In Cancermentioning
confidence: 99%
“…23 Furthermore, a recent study reported the function of AGL in NSCLC and suggested that the silencing of AGL enhanced NSCLC cells' growth, which was mediated by HAS2. 24 Myo-inositol oxygenase (MIOX) was one member of the family consisting of different Aldo-Keto reductases and participated in starting the myo-inositol metabolism.…”
Section: Discussionmentioning
confidence: 99%