ArticleExperimental and therapeutic medicine2021
Silencing of kallikrein-related peptidase 6 attenuates the proliferation, migration, and invasion of gastric cancer cells through inhibition of epithelial-mesenchymal transition.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- The Kallikrein-Kinin System: Proteolytic Orchestrators of Tissue Barrier Disruption in Inflammation and Cancer.International journal of molecular sciences · 2026Review
- A protein-small molecule conjugate as a bispecific inhibitor of proteases implicated in cancer metastasis.Scientific reports · 2026Article
- circRNA_0005927 inhibits gastric cancer metastasis by downregulating the miR-570-3p/FOXO3 axis.American journal of translational research · 2025Article
- A KLK6 Activity-Based Probe Reveals a Role for KLK6 Activity in Pancreatic Cancer Cell Invasion.Journal of the American Chemical Society · 2022Article
- MicroRNA-363-3p, negatively regulated by long non-coding RNA small nucleolar RNA host gene 5, inhibits tumor progression by targeting Aurora kinase A in colorectal cancer.Bioengineered · 2022Article
- Eukaryotic Translation Initiation Factor 5A Independently Predicts Poor Prognosis of Cholangiocarcinoma Patients and Regulates the Ferroptosis and Mitochondrial Apoptosis.Journal of oncology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kallikrein-related peptidase 6 (KLK6), a member of the kallikrein-related peptidase family, is involved in the regulation of epithelial-mesenchymal transition (EMT) in cancer cells and is highly expressed in gastric cancer tissues. The aim of the present study was to investigate the effect of KLK6 on the proliferation, migration and invasion of gastric cancer cells and to determine the underlying mechanism of its actions. The expression of KLK6 was measured in metastatic gastric cancer cells using western blotting and reverse transcription-quantitative PCR, and KLK6 was overexpressed or inhibited in HGC-27 cells using plasmid transfection. Cell proliferation, migration, invasion and EMT were also evaluated using Cell Counting Kit 8, Transwell and western blot analysis, respectively. In addition, a mouse xenograft model was constructed by injection of HGC-27 cells. The xenograft was treated with KLK6 interference or overexpression plasmids to study the
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