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Chronic pepsin exposure promotes anchorage-independent growth and migration of a hypopharyngeal squamous cell line.

Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery (2014-01-01)
Elizabeth A Kelly, Tina L Samuels, Nikki Johnston
ABSTRACT

(1) Investigate the role of reflux, specifically pepsin, in laryngopharyngeal carcinogenesis. (2) Evaluate effects of chronic pepsin exposure on cell migration, apoptosis, and colony-forming ability in hypopharyngeal cells. Translation research. Academic research laboratory. Human hypopharyngeal squamous carcinoma FaDu cells were chronically exposed to nonacidic pepsin (exposed for 24 hours, 4 times over 2 weeks at the following concentrations: 0.01 mg/mL, 0.1 mg/mL, or 1 mg/mL). Precise wounds were created in confluent cell plates, and rates of cell migration into wounds were quantified. Separately, cell viability of chronic pepsin-exposed FaDu cells acutely treated with paclitaxel was measured. Finally, a clonogenic assay was performed on these cells to measure effects of chronic pepsin exposure on colony-forming ability. An increased rate of relative wound density was observed in chronic pepsin-treated (0.01 mg/mL, 0.1 mg/mL) cells compared with control (P < .001), suggesting greater rates of cell migration. Pepsin-treated (0.1 mg/mL) cells demonstrated on average greater cell viability compared with control after exposure to paclitaxel, suggesting possible apoptotic resistance; however, this was not statistically significant. Chronic pepsin exposure (0.1 mg/mL, 1 mg/mL) was associated with a dose-dependent increase in colony-forming ability relative to control (P < .001). Hypopharyngeal squamous cell line chronically exposed to pepsin demonstrated increased cell migration and colony-forming ability relative to control cells. These experiments indicate that chronic pepsin exposure acts as a promoter of tumorigenesis and metastasis of airway epithelium, suggesting a role for pepsin in laryngopharyngeal carcinogenesis attributed to gastric reflux.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
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胃蛋白酶, powder, European Pharmacopoeia (EP) Reference Standard
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胃蛋白酶 来源于猪胃粘膜, powder, slightly beige, ≥500 U/mg
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胃蛋白酶 来源于猪胃粘膜, powder, slightly beige, 1200-2400 U/mg
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胃蛋白酶 来源于猪胃粘膜, Suitable for manufacturing of diagnostic kits and reagents, lyophilized powder, ≥3200 units/mg protein