Purpose: This study was done to confirm the role of NF-kappa B in cisplatin-induced apoptosis of oral squamous cell carcinoma. Materials and Methods: Five cell lines originated from different oral cancer patients were tested for the apoptosis by the treatment of cisplatin. These cells showed different degree of cisplatin-resistance and the order is OSCC-2> OSCC-3> OSCC-5> OSCC-1> OSCC-4. OSCC-2 and OSCC-4 cells were assayed for the apoptosis by measuring DNA fragmentation and TUNEL staining after cisplatin treatment. While OSCC-4 cells showed apoptosis, OSCC-2 cells showed no or very slight apoptosis by cisplatin treatment. Next, It was determined whether NF-kappa B activation is required in mediating cisplatin-induced apoptosis of OSCC-4 . Result: The result was that elevated NF-kappa B activity mediated cisplatin-induced apoptosis. Conclusion: In conclusion, these findings suggest that NF-kappa B activation is essential to cisplatin-induced apoptosis and it may be involved in cisplatin resistance in OSCC cells.
Apoptosis* ; Carcinoma, Squamous Cell* ; Cell Line ; Cisplatin ; DNA Fragmentation ; Humans ; In Situ Nick-End Labeling ; Mouth Neoplasms ; Negotiating ; NF-kappa B*

Purpose: This study was done to confirm the role of NF-kappa B in cisplatin-induced apoptosis of oral squamous cell carcinoma. Materials and Methods: Five cell lines originated from different oral cancer patients were tested for the apoptosis by the treatment of cisplatin. These cells showed different degree of cisplatin-resistance and the order is OSCC-2> OSCC-3> OSCC-5> OSCC-1> OSCC-4. OSCC-2 and OSCC-4 cells were assayed for the apoptosis by measuring DNA fragmentation and TUNEL staining after cisplatin treatment. While OSCC-4 cells showed apoptosis, OSCC-2 cells showed no or very slight apoptosis by cisplatin treatment. Next, It was determined whether NF-kappa B activation is required in mediating cisplatin-induced apoptosis of OSCC-4 . Result: The result was that elevated NF-kappa B activity mediated cisplatin-induced apoptosis. Conclusion: In conclusion, these findings suggest that NF-kappa B activation is essential to cisplatin-induced apoptosis and it may be involved in cisplatin resistance in OSCC cells.
Apoptosis* ; Carcinoma, Squamous Cell* ; Cell Line ; Cisplatin ; DNA Fragmentation ; Humans ; In Situ Nick-End Labeling ; Mouth Neoplasms ; Negotiating ; NF-kappa B*

Background: Exposure to ozone (O3) induces neutrophilic inflammation and goblet cell hyperplasia in humans and experimental animals. Because the solute carrier family 26-member 4 (Slc26a4; pendrin) gene induces mucin production and intraluminal acidification in the airways, it was hypothesized to be a key molecule in O3-induced airway injury. Thus, we evaluated the role of Slc26a4 and the protective effects of ammonium chloride (NH4Cl) in O3 -induced airway injury in mice. Methods: Six-week-old female BALB/c mice were exposed to filtered air or O3 for 21 days (2 ppm for 3 hr/day). NH4Cl (0, 0.1, 1, and 10 mM) was administered intratracheally into the airways. Airway resistance was measured using a flexiVent system, and bronchoalveolar lavage fluid (BALF) cells were differentially counted. Slc26a4 and Muc5ac proteins and mRNA were measured via western blotting, real-time polymerase chain reaction, and immunostaining. Tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-17, IL-1β, and caspase-1 were analyzed via western blotting. Results: The levels Slc26a4 protein and mRNA significantly increased in lung tissues from Day 7 to Day 21 of O3exposure, with concomitant increases in lung resistance, numbers of goblet cells in lung tissues, and inflammatory cells and thiocyanate (SCN− ) levels in BALF in a time-dependent manner. Treatment with NH4Cl significantly reduced these changes to levels similar to those of sham-treated mice, with a concomitant reduction of Slc26a4 proteins in lung lysates and SCN − levels in BALF. Slc26a4 protein was co-expressed with muc5ac protein in the bronchial epithelium, as indicated by immunofluorescence staining. NH4 Cl treatment also significantly attenuated the O3 -induced increases in IFN-γ, TNF-α, IL-17, IL-1β, and p20-activated caspase-1. Conclusion Slc26a4 may be involved in O3 -induced inflammatory and epithelial changes in the airways via activation of the inflammasome and the induction of IL-17 and IFN-γ. NH4 Cl shows a potential as a therapeutic agent for controlling O3 -induced airway inflammation and epithelial damage by modulating Slc26a4 expression.