ArticleJournal of cancer research and clinical oncology2013
Tripeptidyl peptidase II in human oral squamous cell carcinoma.
Article in Journal of cancer research and clinical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Kinesin family member 4A: a potential predictor for progression of human oral cancer.PloS one · 2013Trial
- Mesenchymal stromal/stem cells promote intestinal epithelium regeneration after chemotherapy-induced damage.Stem cell research & therapy · 2024Article
- Identification of Serum Biomarkers to Monitor Therapeutic Response in Intestinal-Type Gastric Cancer.International journal of molecular sciences · 2024Article
- Article
- SYT12 plays a critical role in oral cancer and may be a novel therapeutic target.Journal of Cancer · 2019Article
- Centromere Protein N Participates in Cellular Proliferation of Human Oral Cancer by Cell-Cycle Enhancement.Journal of Cancer · 2019Article
- Evidence for Critical Role of Lymphocyte Cytosolic Protein 1 in Oral Cancer.Scientific reports · 2017Article
- Activin B Regulates Adhesion, Invasiveness, and Migratory Activities in Oral Cancer: a Potential Biomarker for Metastasis.Journal of Cancer · 2017Article
- ARNT2 Regulates Tumoral Growth in Oral Squamous Cell Carcinoma.Journal of Cancer · 2016Article
- Kinesin family member 14 in human oral cancer: A potential biomarker for tumoral growth.Biochemistry and biophysics reports · 2015Article
- Tripeptidyl Peptidase II Mediates Levels of Nuclear Phosphorylated ERK1 and ERK2.Molecular & cellular proteomics : MCP · 2015Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTripeptidyl peptidase II (TPP2), a member of the family of eukaryotic serine peptidase, has been implicated in DNA repair, cellular division, and apoptosis. The aim of this study was to examine TPP2 expression and its functional mechanisms in oral squamous cell carcinoma (OSCC).
methodsTPP2 mRNA and protein expression in seven OSCC-derived cells (Ca9-22, HSC-2, HSC-3, HSC-4, HO-1-N-1, H1, and Sa3) was analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunoblotting analyses. Since previous studies indicated that TPP2 might control chromosomal division, we investigated cellular proliferation and spindle assembly checkpoint (SAC) molecules, MAD2 and CCNB1. In addition, we evaluated the correlation between TPP2 expression levels in primary OSCCs (n = 108 specimens) and the clinicopathologic status by immunohistochemistry (IHC).
resultsTPP2 mRNA and protein were significantly (P < 0.05) up-regulated in OSCC-derived cells compared with human normal oral keratinocytes. Suppression of TPP2 expression with shRNA significantly (P < 0.05) inhibited cellular proliferation compared with the control cells. In addition, appropriate localization of MAD2 and up-regulation of CCNB1 were observed in TPP2 knockdown OSCC cells. IHC showed that TPP2 expression in primary OSCCs was significantly (P < 0.001) greater than that in the normal oral counterparts, and the TPP2-positive cases were significantly (P < 0.05) correlated with tumor size.
conclusionThe current study showed that overexpression of TPP2 occurs frequently during oral carcinogenesis and might be associated with OSCC progression via SAC activation.
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