When Anticancer Agents Are Applied to Adenocarcinoma Cells, Platelets Improve Their Survival Rate Medications: Mechanisms and Chemoresistance Implications

Overview and Goals: Cancer cells are more likely to survive when they are not constrained by feedback control mechanisms. Chemosis and persistent side effects from chemotherapy might make cancer treatment more difficult to manage tumor cells' ability to survive. In this study, we looked at how platelets affect the survival and death of cancer cells treated with chemotherapy AN EXPERIMENTAL METHOD: Human adenocarcinoma cells, namely colonic (Caco-2) and ovarian (59 M) cells, were cultured for 1, 24, or 72 hours with or without platelets (1.5 · 108 mL-1). The drugs used were 5-fluorouracil (1–300 mg·mL–1) or paclitaxel (1–200 mg·mL–1). After incubation, cancer cells were isolated and used flow cytometry, Western blotting, real-time PCR, TaqMan® Gene Expression Assays, and proteomics to determine if the cells had survived or died ESSENTIAL OUTCOMES: Human platelets multiplied the ability of colonic and ovarian adenocarcinoma cells treated with 5-fluorouracil and paclitaxel, two common anticancer medications, to survive. Cancer cells expressed more cyclins, DNA repair proteins, and MAPKs when platelets were present. They also down- and up-regulated pro- and anti-apoptotic genes, increased the number of cells synthesizing DNA, and decreased the number in the quiescent phase. The thrombospondin-1, TGF-b, clustering, and chemokine RANTES were released, according to an investigation of the platelet-Caco-2 secretum. Lastly, thrombospondin-1 and human recombinant RANTES increased the ability of Caco-2 cells exposed to paclitaxel to survive SUMMARY AND IMPLICATIONS These findings show that platelets boost the survival, growth, and chemoresistance of adenocarcinoma cells to conventional anticancer medications. Changing the connections between cancer cells and platelets may be a fresh approach to raising the effectiveness of chemotherapy.