No abstract
The tumor microenvironment that refers to the tumour’s surroundings is a key modulator of tumor growth and invasion. The tumour derived signals are known to downregulate the anti-tumor effects of the effector cells present in the TME. Thus, the cross talk between the tumor cells with the surrounding immune cells helps in evading the tumor surveillance as well as aiding in tumor growth and proliferation. Hence, knowledge regarding the effects of drugs/compound on the tumor-stromal interactions are gaining importance. In the present study, the effects of jacalin, a dietary lectin on the proliferation and cytokine production of peripheral blood mononuclear cells (PBMCs) are investigated. Jacalin was shown to act as a mitogen of PBMCs, the key cytokine secreting immune cells. Also, jacalin initially induces increased mRNA expression of pro-inflammatory cytokine IFN-γ; however prolonged stimulation of PBMCs resulted in increased expression of anti-inflammatory cytokine, mainly TGF-β. Further, 6 h jacalin prestimulated PBMCs (Jac-PBMCs) were shown to inhibit HeLa cell proliferation while 24 h (Jac-PBMCs) were found to favor tumor growth. Thus, it may be postulated that while jacalin initially polarizes the PBMCs to hinder the tumor growth, after a stipulated time point, interaction of jacalin with PBMCs can lead to an immunosuppressive TME that may probably assist in tumor growth and progression.
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