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Year : 2013  |  Volume : 9  |  Issue : 4  |  Page : 624-629

HSP70 induces TLR4 signaling in oral squamous cell carcinoma: An immunohistochemical study

1 Department of Oral Pathology, Maratha Mandal's NGH Institute of Dental Sciences, Belgaum, Karnataka, India
2 Department of Microbiology, Maratha Mandal's NGH Institute of Dental Sciences, Belgaum, Karnataka, India

Correspondence Address:
Sindhu Nair
Department of Oral Pathology, M.M.N.G.H institute of dental sciences and research centre, Belgaum - 590 010, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-1482.126460

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Objectives: Toll like receptors play an important role in innate and adaptive immune responses. Heat shock proteins play a significant role in cell proliferation, differentiation and oncogenesis. HSP70 acts as one of the ligands of TLR4 and binds to it in a CD14 dependent fashion to bring about proinflammatory cytokine production leading to an anti-tumor response. On the contrary, TLR4 has been implicated in carcinogenesis by secretion of anti-apoptotic proteins. Thus the aim of this study was to compare and correlate the association of HSP70 and TLR4 in various grades of oral squamous cell carcinoma. Study Design: Twenty-seven cases of oral squamous cell carcinoma were considered. Ten cases each of well-differentiated (WDSCC) and moderately differentiated (MDSCC), 7 cases of poorly differentiated carcinoma (PDSCC) were considered. Sections were stained for HSP70 and TLR4 and were evaluated for staining degree and intensity. Results and Conclusion: Positive expression of both HSP70 and TLR4 was found in all cases of WDSCC and MDSCC, whereas in PDSCC out of 7 cases only 6 showed positivity for TLR4 and 4 cases showed positivity for HSP70. Those cases that were positive for TLR4, also showed positivity for HSP70. HSP70 acts as a ligand and binds to TLR4 thus activating the My88 pathway resulting in production of proinflammatory cytokines, chemokines, growth factors etc., enhancing anti-cancer immunity in the early stages of disease. In later stages, TLRs expressed on cancer cells can produce anti-apoptotic proteins contributing to carcinogenesis and cancer cell proliferation.

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