Assignment&lt;footref rid="foot01"&gt;&lt;sup&gt;1&lt;/sup&gt;&lt;/footref&gt; of the dipeptidyl peptidase III gene (DPP3) to human chromosome 11 band q12→q13.1 by in situ hybridization

Fukasawa, Katsuhiko; Fukasawa, Kazuhiro; Harada, Misuzu

doi:10.1159/000015498

Cited by 6 publications

(2 citation statements)

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“…Exopeptidase dipeptidyl peptidase 3 (DPP3) is a member of the zinc-dependent M49 metallopeptidase family that cleaves dipeptides at the N-terminal site 11 , 12 . Human DPP3, a 29,647 bp gene (NC_000011.10), located on chromosome 11q12-13.1 13 . The primary biological function of DPP3 is to regulate the transformation of enkephalin, opioid peptide, terminal protein, and cell signaling 11 .…”

Section: Introductionmentioning

confidence: 99%

DPP3/CDK1 contributes to the progression of colorectal cancer through regulating cell proliferation, cell apoptosis, and cell migration

et al. 2021

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At present, colorectal cancer (CRC) has become a serious threat to human health in the world. Dipeptidyl peptidase 3 (DPP3) is a zinc-dependent hydrolase that may be involved in several physiological processes. However, whether DPP3 affects the development and progression of CRC remains a mystery. This study is the first to demonstrate the role of DPP3 in CRC. Firstly, the results of immunohistochemistry analysis showed the upregulation of DPP3 in CRC tissues compared with normal tissues, which is statistically analyzed to be positively correlated with lymphatic metastasis, pathological stage, positive number of lymph nodes. Moreover, the high expression of DPP3 predicts poor prognosis in CRC patients. In addition, the results of cell dysfunction experiments clarified that the downregulation of DPP3 significantly inhibited cell proliferation, colony formation, cell migration, and promoted apoptosis in vitro. DPP3 depletion could induce cell apoptosis by upregulating the expression of BID, BIM, Caspase3, Caspase8, HSP60, p21, p27, p53, and SMAC. In addition, downregulation of DPP3 can reduce tumorigenicity of CRC cells in vivo. Furthermore, CDK1 is determined to be a downstream target of DPP3-mediated regulation of CRC by RNA-seq, qPCR, and WB. The interaction between DPP3 and CDK1 shows mutual regulation. Specifically, downregulation of DPP3 can accentuate the effects of CDK1 knockdown on the function of CRC cells. Overexpression of CDK1 alleviates the inhibitory effects of DPP3 knockdown in CRC cells. In summary, DPP3 has oncogene-like functions in the development and progression of CRC by targeting CDK1, which may be an effective molecular target for the prognosis and treatment of CRC.

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Section: Introductionmentioning

confidence: 99%

DPP3/CDK1 contributes to the progression of colorectal cancer through regulating cell proliferation, cell apoptosis, and cell migration

et al. 2021

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“…hDPP III gene (http://www.ncbi.nlm.nih.gov/nuccore/NC_000011.9) containing 18 exons and 17 introns is located on chromosome 11q12‐13.1 [83]. Although eight putative mRNA transcripts ranging from 1382 to 3370 bp have been predicted (Ensembl), only two of them, namely variant I (2694 bp, http://www.ncbi.nlm.nih.gov/nuccore/NM_005700) and variant II (2697 bp, http://www.ncbi.nlm.nih.gov/nuccore/NM_130443), have been cloned and characterized [43,84–86].…”

Section: Physicochemical Propertiesmentioning

confidence: 99%

Dipeptidyl peptidase III: a multifaceted oligopeptide N‐end cutter

2011

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Dipeptidyl peptidase III (DPP III), the sole member and representative of the M49 family of metallopeptidases, is a zinc-dependent aminopeptidase. It sequentially hydrolyses dipeptides from the N-terminal of oligopeptides ranging from three to 10 amino acid residues. Although implicated in an array of pathophysiological phenomena, the precise function of this peptidase is still unclear. However, a number of studies advocate its contribution in terminal stages of protein turnover. Altered expression of DPP III which suggests its involvement in primary ovarian carcinoma, oxidative stress (Nrf2 nuclear localization), pain, inflammation and cataractogenesis has recently led to resurgence of interest in delineating the role of the peptidase in these pathophysiological processes. This review article intends to bring forth the latest updates in this arena which may serve as a base for future studies on the peptidase.

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Dipeptidyl Peptidases

Thiele

2002

Wiley Encyclopedia of Molecular Medicine

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Assignment<footref rid="foot01"><sup>1</sup></footref> of the dipeptidyl peptidase III gene (DPP3) to human chromosome 11 band q12→q13.1 by in situ hybridization

Cited by 6 publications

References 4 publications

DPP3/CDK1 contributes to the progression of colorectal cancer through regulating cell proliferation, cell apoptosis, and cell migration

DPP3/CDK1 contributes to the progression of colorectal cancer through regulating cell proliferation, cell apoptosis, and cell migration

Dipeptidyl peptidase III: a multifaceted oligopeptide N‐end cutter

Dipeptidyl Peptidases

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