Abstract
In the last decade, it has become apparent that toll-like receptor (TLR) signaling can play an important role in ovarian cancer (OC) progression. Interestingly, TLR activation in immune cells can help activate an anti-tumor response, while TLR signaling in tumor cells themselves is often associated with cancer-promoting inflammation. For example, it has been shown that TLR activation in dendritic cells can result in more effective antigen presentation to T cells, thereby favoring tumor eradication. However, aberrant TLR expression in OC cells is associated with more aggressive disease (likely due to recruitment of pro-tumoral leukocytes to the tumor site) and has also been implicated in resistance to mainstream chemotherapy. The delicate balance of TLR activation in the tumor microenvironment in different cell types altogether help shape the inflammatory profile and outcome of tumor growth or regression. With further studies, specific activation or repression of TLRs may be harnessed to offer novel immunotherapies or adjuvants to traditional chemotherapy for some OC patients. Herewith, we review recent literature on basic and translational research concerning therapeutic targeting of TLR pathways for the treatment of OC.
Highlights
Ovarian cancer (OC) has the most devastating death rate of gynecological cancers with only 44% of women surviving 5 years after diagnosis [1,2,3,4]
We summarize recent studies and clinical trials aimed at exploiting toll-like receptor (TLR) signaling pathways for OC immunotherapy
CONCLUDING REMARKS The last decade of research on TLR activity and its implications in OC progression indicate that inhibition of certain TLRs in cancer cells and/or TLR stimulation in immune cells may be of therapeutic benefit in some patients
Summary
Ovarian cancer (OC) has the most devastating death rate of gynecological cancers with only 44% of women surviving 5 years after diagnosis [1,2,3,4]. As aggressive OC often correlates with an immunosuppressive leukocyte population in the tumor environment, efforts to modulate these cells to potentiate an anti-tumor immune response are ongoing [10,11,12]. TLR expression is well-established in immune cells, such as macrophages and dendritic cells (DCs), where upon PAMP recognition, an inflammatory response occurs, activating numerous transcription factors, such as NF-kB and IRF 3/7 [21,22,23].
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