Role of Toll like receptor in progression and suppression of oral squamous cell carcinoma

Abstract

Oral squamous cell carcinoma (OSCC) is one of the most common type of head and neck squamous cell carcinoma and one of the multifactorial process that consists of most contributing factors such as tobacco smoking, chewing and alcohol consumption that altered the intracellular environment. Recent studies have shown relevance of Toll like receptor (TLR) associated with carcinogenesis. This review aim’s to explore that how TLR associates with progression and suppression of OSCC. This review is a classical review that has confined to articles published in the past 19 years (i.e. 2000-2019) and has summarized the perspective of the authors. 62 articles were reviewed and it was found that progression and suppression of OSCC is associated with different TLRs promoting tumor development and also inhibiting the progression of oral neoplasm. It was found that TLR2, TLR3, TLR4, TLR5, TLR7 and TLR9 are associated with tumor development i.e. in progression of OSCC, where as suppression of OSCC through TLR3 and TLR7. We authors would like to conclude that literature survey has indicated effective TLR’s against OSCC development and can be explored to investigate other TLRs that can be used for therapeutic purposes in near future.

Protein overexpression of toll‑like receptor 4 and myeloid differentiation factor 88 in oral squamous cell carcinoma and clinical significance

“…In the present study, a significant increase in the expression of TLR4 and MyD88 in OSCC was observed. This result is consistent with the results of Sharma and Bala ( 38 ). The TLR4/MyD88 signaling pathway activates the expression of NF-κB ( 39 ) and secondarily promotes the expression of pro-inflammatory genes, thereby triggering the inflammatory response of the host.…”

“…This suggests that overexpression of MyD88 is involved in tumor differentiation. The results are consistent with the results of Sharma and Bala ( 38 ), who also reported that high expression of TLR4 was associated with deep tumor invasion. He et al ( 42 ) indicated that activation of the TLR4-MyD88-NF-κB signaling pathway may stimulate epithelial-mesenchymal transition (EMT), which allows cancer cells to detach from the primary site and then invade lymphatic and/or blood vessels, resulting in loss of epithelial adhesion and polarity of cancer cells and promote tumor metastasis.…”

“…In the present study, a significant increase in the expression of TLR4 and MyD88 in OSCC was observed. This result is consistent with the results of Sharma and Bala (38).The TLR4/MyD88 signaling pathway activates the expression of NF-κB (39) and secondarily promotes the expression of pro-inflammatory genes, thereby triggering the inflammatory response of the host. When activated by TLR4 through stress, injury, death of cells or degradation of extracellular matrix, two signaling pathways are activated, of which the MyD88-dependent pathway is activated in a series of ways, and finally, the NF-κB signaling pathway is activated.…”

Prognostic value of immune-related genes in laryngeal squamous cell carcinoma

“…Previous studies have shown that TLR2 was connected with occurrence and prognosis of LSCC (19). TLR2 signaling pathway was found to be involved in promoting tumor cell movement via activation of the NF-κB pathway in breast and oral cancer (20,21).…”

“…Previous studies have shown that TLR2 was connected with occurrence and prognosis of LSCC ( 19 ). TLR2 signaling pathway was found to be involved in promoting tumor cell movement via activation of the NF-κB pathway in breast and oral cancer ( 20 , 21 ). In addition to gastric cancer, high expression of TLR2 was related to up-regulation anti-apoptotic and down-regulation tumor suppressor genes, which predicts poor prognosis ( 22 ).…”