The tumor microenvironment that refers to the
tumor's surroundings is a key modulator of
tumor growth and invasion. The
tumor-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 is 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 induced 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. Furthermore, 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.