ArticleScientific reports2015
NES1/KLK10 gene represses proliferation, enhances apoptosis and down-regulates glucose metabolism of PC3 prostate cancer cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- ADAMTS-8 and kallikrein-related peptidases 10 and 5 proteases also have a tumor suppression role.World journal of clinical oncology · 2025Review
- Salivary Proteome Is Altered in Children With Small Area Thermal Burns.Proteomics. Clinical applications · 2025Article
- MicroRNA-141-regulated KLK10 and TNFSF-15 gene expression in hepatoblastoma cells as a novel mechanism in liver carcinogenesis.Scientific reports · 2024Article
- LRG1 promotes the apoptosis of pulmonary microvascular endothelial cells through KLK10 in chronic obstructive pulmonary disease.Tobacco induced diseases · 2024Article
- Multidimensional outlook on the pathophysiology of cervical cancer invasion and metastasis.Molecular and cellular biochemistry · 2023Review
- Comprehensive analyses of circulating cardiometabolic proteins and objective measures of fat mass.International journal of obesity (2005) · 2023Article
- Ovol1/2 loss-induced epidermal defects elicit skin immune activation and alter global metabolism.EMBO reports · 2023Article
- Molecular characterization of epithelial-mesenchymal transition and medical treatment related-genes in non-functioning pituitary neuroendocrine tumors.Frontiers in endocrinology · 2023Article
- A Pair of Prognostic Biomarkers in Triple-Negative Breast Cancer: KLK10 and KLK11 mRNA Expression.Life (Basel, Switzerland) · 2022Article
- Effects of iron modulation on mesenchymal stem cell-induced drug resistance in estrogen receptor-positive breast cancer.Oncogene · 2022Article
- Ecdysoneless Protein Regulates Viral and Cellular mRNA Splicing to Promote Cervical Oncogenesis.Molecular cancer research : MCR · 2022Article
- Stable flow-induced expression of KLK10 inhibits endothelial inflammation and atherosclerosis.eLife · 2022Article
- Emerging Proteins in CRPC: Functional Roles and Clinical Implications.Frontiers in oncology · 2022Review
- Angiotensin receptor-neprilysin inhibitor improves coronary collateral perfusion.Frontiers in cardiovascular medicine · 2022Article
- Transcriptional Suppression of miR-7 by MTA2 Induces Sp1-Mediated KLK10 Expression and Metastasis of Cervical Cancer.Molecular therapy. Nucleic acids · 2020Article
- NES1/KLK10 and hNIS gene therapy enhanced iodine-131 internal radiation in PC3 proliferation inhibition.Frontiers of medicine · 2019Article
- Review
- Radiosensitizing effects of Sestrin2 in PC3 prostate cancer cells.Iranian journal of basic medical sciences · 2018Article
- KLK10 exon 3 unmethylated PCR product concentration: a new potential early diagnostic marker in ovarian cancer? - A pilot study.Journal of ovarian research · 2018Article
- Elevated tumor tissue protein expression levels of kallikrein-related peptidases KLK10 and KLK11 are associated with a better prognosis in advanced high-grade serous ovarian cancer patients.American journal of cancer research · 2018Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The normal epithelial cell-specific-1 (NES1) gene, also named as KLK10, is recognised as a novel putative tumour suppressor in breast cancer, but few studies have focused on the function of KLK10 in human prostate cancer. Our study confirms that the expression of KLK10 in prostate cancer tissue and cell lines (PC3, DU145, and LNCaP clone FGC) is low. Given that the androgen-independent growth characteristic of the PC3 cell line is more similar to clinical castration-resistant prostate cancer, we studied the role of KLK10 in PC3. In vitro and in vivo assays showed that over-expressing KLK10 in PC3 could decelerate tumour proliferation, which was accompanied with an increase in apoptosis and suppression of glucose metabolism. The related proteins, such as Bcl-2 and HK-2, were down-regulated subsequently. Furthermore, by up-regulating Bcl-2 or HK-2 respectively in the PC3-KLK10 cell line, we observed a subsequent increase of cell proliferation and a synchronous up-regulation of HK-2 and Bcl-2. Besides, KLK10 expression was also increased by Bcl-2 and HK-2, which suggests that there is a negative feedback loop between KLK10 and Bcl-2/HK-2. Thus, our results demonstrated that KLK10 may function as a tumour suppressor by repressing proliferation, enhancing apoptosis and decreasing glucose metabolism in PC3 cells.
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