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Identification of proteins that interacted with DPYSL2

ABSTRACT: Dihydropyrimidinase like 2 promotes bladder cancer progression via pyruvate kinase M2-induced aerobic glycolysis and epithelial–mesenchymal transition. DPYSL2 promotes bladder cancer progression via PKM2.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture, Kidney

DISEASE(S): Disease Free,Urinary Bladder Cancer

SUBMITTER: Sun Tianyong

LAB HEAD: Jun Zou

PROVIDER: PXD023279 | Pride | 2021-09-09

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	NC1-DB-search-psm.csv	Csv
	NC1-peptides.html	Other
	NC1-protein.html	Other
	NC1.wiff	Wiff
	NC2-5-DB-search-psm.csv	Csv

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Publications

Dihydropyrimidinase Like 2 Promotes Bladder Cancer Progression via Pyruvate Kinase M2-Induced Aerobic Glycolysis and Epithelial-Mesenchymal Transition.

Zou Jun J Huang Ruiyan R Chen Yanfei Y Huang Xiaoping X Li Huajun H Liang Peng P Chen Shan S

Frontiers in cell and developmental biology 20210706

<h4>Background</h4>Aerobic glycolysis and epidermal-mesenchymal transition (EMT) play key roles in the development of bladder cancer. This study aimed to investigate the function and the underlying mechanism of dihydropyrimidinase like 2 (DPYSL2) in bladder cancer progression.<h4>Methods</h4>The expression pattern of DPYSL2 in bladder cancer and the correlation of DPYSL2 expression with clinicopathological characteristics of bladder cancer patients were analyzed using the data from different dat ...[more]

PMID: 34295887

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Germline loss of PKM2 promotes metabolic distress and hepatocellular carcinoma

Project description:Alternative splicing of the Pkm gene product generates the PKM1 and PKM2 isoforms of pyruvate kinase, and PKM2 expression is closely linked to embryogenesis, tissue regeneration, and cancer. To interrogate the functional requirement for PKM2 during development and tissue homeostasis, we generated germline PKM2 null mice (Pkm2-/-). Unexpectedly, despite being the primary isoform expressed in most wild-type adult tissues, we found that Pkm2-/- mice are viable and fertile. Thus, PKM2 is not required for embryonic or postnatal development. Loss of PKM2 leads to compensatory expression of PKM1 in the tissues that normally express PKM2. Strikingly, PKM2 loss leads to spontaneous development of hepatocellular carcinoma (HCC) with high penetrance that is accompanied by progressive changes in systemic metabolism characterized by altered systemic glucose homeostasis, inflammation, and hepatic steatosis. Therefore, in addition to its role in cancer metabolism, PKM2 plays a role in controlling systemic metabolic homeostasis and inflammation, thereby preventing HCC by a non-cell-autonomous mechanism. RNA was isolated from flash frozen ground whole liver tissue of 35 week old PKM2 KO and WT mice. Three independent mice from each condition were used as biological replicates.

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