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findings show that KLK10 promotes trastuzumab resistance, at least in part, through the PI3K/AKT signaling pathway, suggesting that KLK10 is a potentially target to overcome trastuzumab resistance, and the combination might overcome trastuzumab resistance in KLK10-overexpressed gastric cancer patients.
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MiR-199b-5p promotes cell proliferation, migration and suppresses apoptosis in cervical cancer cells. KLK10 is a direct target of miR-199b-5p. MiR-199b-5p expression is increased and positively correlated with KI-67 in human cervical cancer tissues and cell lines.
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blockade of KLK10 attenuates epithelial-mesenchymal transition and activation of FAK-SRC-ERK signaling, which explains the mechanism of KLK10 in promoting metastasis.
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To the best of our knowledge, this is the first report on KLK10 exon 3 unmethylated PCR product concentration as potential early epigenetic diagnostic marker in primary ovarian tumors.
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KLK10 was verified to be a potential therapeutic target for reversing trastuzumab resistance in breast cancer cells.
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Pronounced correlations between KLK10/KLK11 (rs = 0.647) and between KLK9/KLK15 (rs = 0.716) mRNA, but not between other combinations, indicate coordinate expression of distinct pairs of peptidases
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identification and molecular cloning of eight novel transcripts of the human KLK10 gene using 3' rapid amplification of cDNA ends (3' RACE) and next-generation sequencing (NGS), as well as their expression analysis in a wide panel of cell lines, originating from several distinct cancerous and normal tissues
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Data suggest that mature KLK9 (kallikrein 9) is a glycosylated chymotrypsin-like enzyme with strong preference for tyrosine over phenylalanine at P1 cleavage position; substrate specificity of KLK9 appears to extend to KLK10 and midkine; enzyme activity is enhanced by Mg2+ and Ca2+, but is reversibly attenuated by Zn2+; KLK9 is inhibited in vitro by many naturally occurring or synthetic protease inhibitors.
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KLK10 potentially plays a crucial role in esophageal cancer cell growth.
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KLK10 may function as a tumour suppressor by repressing proliferation, enhancing apoptosis and decreasing glucose metabolism in PC3 cells.
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treated and untreated prolactin-producing pituitary adenomas and carcinomas as well as TSH-producing pituitary adenomas and carcinomas were conclusively immunopositive for KLK10
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Immunoexpression of KLK10 in the ACTH-secreting tumors as well as in the Crooke cell tumors was significantly increased when compared with the nonfunctioning tumors and in the corticotrophs of non-tumorous pituitaries.
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Data indicate that elevated expression of microRNA-375 in head and neck squamous cell carcinoma (HNSCC) cells significantly reduces kallikrein 6 (KLK6), kallikrein 10 (KLK10), and matrix metalloproteinase 9 (MMP9) messenger RNA expression.
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is the first correlation of oral squamous cell carcinoma with KLK10 rs3745535G>T polymorphisms
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KLK6 and KLK10 may be useful markers and potential therapeutic targets in gastroesophageal junction tumors
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This study assessed the prognostic utility of human tissue kallikrein-like peptidases 6 and 10 (KLK6 and KLK10) and correlated their expression with histopathological and clinical parameters in gastric cancer.
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KLK10 expression is an independent biomarker of unfavorable prognosis in patients with gastric cancer.
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Patients with high KLK10 expression had a shorter disease-free and overall survival rates.
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Enhancing KLK10 gene expression can decrease the proliferation and invasiveness of human tongue cancer cells in vitro.
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Finding lower KLK10 levels in pleomorphic adenoma suggests aberrant expression in a tumour that develops primarily from myoepithelial cells. A kallikrein cascade may play a role in the development and/or outcome of some salivary gland tumours.
