Activation Toll-Like Receptor7 (TLR7) Responsiveness Associated with Mitogen- Activated Protein Kinase (MAPK) Activation in HIOEC Cell Line of Oral Squamous Cell Carcinoma

• Main Authors: Ali Mahmoud Hashemi, Hamid Mahmoud Hashemi, Shiva Solahaye Kahnamouii, Talieh Mahmoud Hashemi, Hassan Agajani, Khalil Frozannia, Alireza Pournasrollah, Rasoul Sadeg, Rasoul Estakhri, Ebrahim Razmpa, Naghmeh Bahrami
• Format: Article
• Language: English
• Published: Shiraz University of Medical Sciences 2018-09-01
• Series: Journal of Dentistry
• Subjects: Toll-Like Receptor 7 ● Mitogen-Activated Protein Kinase ● Squamous Cell Carcinoma
• Online Access: http://dentjods.sums.ac.ir/index.php/JDSUMS/article/view/1723/1134

Statement of the Problem: Oral squamous cell carcinoma is the most common oral malignancy. Toll-like receptor (TLR) activation led to alterations in the levels of mRNA encoding the TLR accountable for recognizing the inducing agonist and cross-regulation of other TLR. Purpose: The purpose of this study is determination of mitogen-associated protein kinase (MAPK) activation in human immortalized oral epithelial cell (HIOEC) line via up regulating of TLR7. Materials and Method: expression of TLR7 was measured in HIOEC and normal cells by quantitative real-time polymerase chain reaction (qRT-PCR) and samples were calibrated by β-actin. Results: Western blot analysis discovered high expression of TLR7 and MAPK in HIOEC cell lines. TLR7 was over-expressed in HIOEC cell line. Imiquimod-induced expression of interleukin (IL)-6, IL-8, and vascular endothelial growth factor (VEGF) was inhibited by TLR7 siRNA in HIOEC cells as determined by reverse transcription polymerase chain reaction (RT-PCR). Mean fluorescence intensity of nuclear p38 expression was determined in HIOEC cell lines (p< 0.05). RT-PCR analysis of IL-6, IL-8, and VEGF mRNA expression in HIOEC cells stimulated with imiquimod (1 μg/ml) for indicated time points. Conclusion: TLR7 is functionally over-expressed in HIOEC cell line of oral squamous cell carcinoma and development of resistance to cisplatin in human oral squamous cell carcinoma might occur through the mechanism involving activation of TLR7 and its dependent signaling pathway.