[The molecular mechanism between interstitial fluid pressure and malignant phenotype of salivary adenoid cystic carcinoma].

OBJECTIVE: To explore the effects of stress imposed on adenoid cystic carcinoma (ACC), therefore to clarify the molecular basis and mechanism of ACC's malignant phenotype under the elevated tumor interstitial fluid pressure. METHODS: ACC cells were cultured under pressure (103.74 kPa), and were divided into four groups (3 h group, 6 h group, 12 h group, 24 h group) according the pressure time. Untreated ACC2 was as negative control group, untreated ACCM was as positive control group. The level of epidermal growth factor receptor (EGFR) was detected by semiquantitative analysis of immunochemistry. Matrix metalloproteinase 9 (MMP9) and EGFR mRNA expression were assessed by reverse transcriptase polymerase chain reaction. EGFR, phosphorylation epidermal growth factor receptor (P-EGFR), MMP9, keratinocyte growth factor (KGF) and phosphorylation extracellular signal-regulated kinase (P-ERK) protein expressions were assessed by Western blot. RESULTS: As the extension of pressure time, the expression of EGFR, P-EGFR, MMP9, KGF, P-ERK in ACC2 gradually increased, which were positive correlation with pressure time, and were higher than that of negative control group. CONCLUSION: Under the stimulation of pressure, the mRNA and protein levels of adhesion molecules and metastatic relative molecules in ACC2 were sharply elevated.