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Extracellular acidity‑induced expression of Kallikrein‑related peptidases 7 and 8 is involved in increased invasiveness of gastric cancer cells
- Source :
- Oncology Reports.
- Publication Year :
- 2020
- Publisher :
- Spandidos Publications, 2020.
-
Abstract
- In several cancers, the acidic microenvironment of cancer cells has been implicated in enhanced malignancy and metastasis. In the present study, it was observed that gastric cancer cell lines, SNU601 and AGS, exposed to an acidic medium had increased invasiveness, as assessed using Matrigel‑coated Transwell analysis. The factors regulating such acidity‑mediated enhancement of invasiveness were investigated and it was revealed that a low‑pH environment markedly increased kallikrein‑related peptidase 7 (KLK7) and kallikrein‑related peptidase 8 (KLK8) expression. Gene silencing assays confirmed that these peptidases were involved in acidity‑promoted invasion. Acidic conditions also increased the expression of cyclooxygenases (COX), key regulatory enzymes in the catalytic pathway of prostaglandin production. Notably, these enzymes appeared to be involved in the acidity‑mediated expression of KLK7 and KLK8, as revealed using COX inhibitors. Therefore, it was indicated that tumor invasion enhancement by extracellular acidity is regulated at least in part through the induction of the COX/KLK7 and KLK8 axis in gastric cancer cells.
- Subjects :
- 0301 basic medicine
Cancer Research
Cell
Cell Culture Techniques
Metastasis
03 medical and health sciences
0302 clinical medicine
Cell Movement
Stomach Neoplasms
Cell Line, Tumor
medicine
Extracellular
Humans
Gene silencing
Neoplasm Invasiveness
Gene Silencing
Oncogene
Chemistry
Cancer
General Medicine
Kallikrein
Hydrogen-Ion Concentration
medicine.disease
Culture Media
Up-Regulation
Gene Expression Regulation, Neoplastic
030104 developmental biology
medicine.anatomical_structure
Oncology
Prostaglandin-Endoperoxide Synthases
030220 oncology & carcinogenesis
Cancer cell
Cancer research
Kallikreins
Subjects
Details
- ISSN :
- 17912431 and 1021335X
- Database :
- OpenAIRE
- Journal :
- Oncology Reports
- Accession number :
- edsair.doi.dedup.....c1c17d99fdaf323ecac96ab65fe6e831