TF/FVIIa/PAR2 promotes cell proliferation and migration via PKCα and ERK-dependent c-Jun/AP-1 pathway in colon cancer cell line SW620

Tumor Biology ◽  
2013 ◽  
Vol 34 (5) ◽  
pp. 2573-2581 ◽  
Author(s):  
Lichao Hu ◽  
Longfei Xia ◽  
Hong Zhou ◽  
Biao Wu ◽  
Yuan Mu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Line ◽  
Cancer Cell ◽  
Cancer Cell Line ◽  
Colon Cancer Cell Line ◽  
Colon Cancer Cell ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Cloning of a novel EGFR-related peptide: a putative negative regulator of EGFR

2001 ◽  
Vol 280 (5) ◽  
pp. C1083-C1089 ◽  
Author(s):  
Yingjie Yu ◽  
Arun K. Rishi ◽  
Jerrold R. Turner ◽  
Dayou Liu ◽  
Eric D. Black ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Line ◽  
Cancer Cell ◽  
Marked Reduction ◽  
Cancer Cell Line ◽  
Colon Cancer Cell Line ◽  
Colon Cancer Cell ◽  
Negative Regulator ◽  
Rat Tissues

Although epidermal growth factor receptor (EGFR) plays a key role in regulating cell proliferation, differentiation, and transformation in many tissues, little is known about the factor(s) that may modulate its function. We have isolated a cDNA clone from the rat gastroduodenal mucosa whose full length revealed 1,958 bp that contained 227 bp of 5′-untranslated region (UTR) and an open-reading frame encoding 479 amino acids, followed by 290 bp of 3′-UTR. It showed ∼85% nucleotide homology to the external domain of the rat EGFR. We refer to the product of the newly isolated cDNA as EGFR-related protein (ERRP). In Northern blot analysis with poly(A)+ RNA from different rat tissues, ERRP cDNA hybridized to several mRNA transcripts with the strongest reaction noted with a transcript of ∼2 kb. Maximal expression of the 2-kb mRNA transcript was observed in the small intestine, followed by colon, liver, gastric mucosa, and other tissues. Transfection of ERRP cDNA into a colon cancer cell line, HCT116, resulted in a marked reduction in proliferation in monolayer and colony formation in soft agar compared with the vector-transfected controls. In another colon cancer cell line, Caco-2, with a tetracycline-regulated promoter system, induction of ERRP expression in the absence of doxycycline was associated with a marked reduction in EGFR activation and proliferation. We conclude that the ERRP cDNA may represent a new member of the EGFR gene family and that ERRP plays a role in regulating cell proliferation by modulating the function of EGFR.

scholarly journals The atypical cyclin CNTD2 promotes colon cancer cell proliferation and migration

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Abril Sánchez-Botet ◽  
Laura Gasa ◽  
Eva Quandt ◽  
Sara Hernández-Ortega ◽  
Javier Jiménez ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Citrate synthase desuccinylation by SIRT5 promotes colon cancer cell proliferation and migration

2020 ◽  
Vol 401 (9) ◽  
pp. 1031-1039
Author(s):  
Mengmeng Ren ◽  
Xin Yang ◽  
Juntao Bie ◽  
Zhe Wang ◽  
Minghui Liu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Enzymatic Activity ◽  
Cancer Cell ◽  
Citrate Synthase ◽  
Colon Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

AbstractCitrate synthase (CS), the rate-limiting enzyme in the tricarboxylic acid (TCA) cycle catalyzes the first step of the cycle, namely, the condensation of oxaloacetate and acetyl-CoA to produce citrate. The expression and enzymatic activity of CS are altered in cancers, but posttranslational modification (PTM) of CS and its regulation in tumorigenesis remain largely obscure. SIRT5 belongs to the nicotinamide adenine dinucleotide (NAD)+-dependent deacetylase sirtuin family and plays vital roles in multiple biological processes via modulating various substrates. Here, we show that SIRT5 interacts with CS and that SIRT5 desuccinylates CS at the evolutionarily conserved residues K393 and K395. Moreover, hypersuccinylation of CS at K393 and K395 dramatically reduces its enzymatic activity and suppresses colon cancer cell proliferation and migration. These results provide experimental evidence in support of a potential therapeutic approach for colon cancer.

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