Immunopotentiation of galangal (Alpinia galanga L.) when combined with T-cells against metastatic triple-negative breast cancer, MDA-MB 231

This study explores the potency of galangal (Alpinia galanga L.) in enhancing the cytotoxic effects of cytotoxic T-cells to suppress the growth of human triple-negative breast cancer cells. T-cells were isolated from peripheral blood mononuclear cells of healthy women and activated with CD3/CD28 T-cell activator to generate the cytotoxic subset of T-cells. The cells were incubated under standard conditions for 10 days. Galangal extract (GE) was subjected to a cytotoxicity test using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to measure its effect on activated T-cells. The effect of GE on activated T-cell differentiation was traced using flow cytometry. The effects of cytotoxic T-cells and GE on MDA-MB-231 cell growth were assayed using MTT assay. For the in silico assay, the natural compounds present in A. galanga L, such as acetoxychavicol acetate, galangin, β-caryophyllene, and p-coumaryl alcohol, were drawn using ChemDraw software, and the conformation series were generated using LowModeMD. The crystal structure of the complex of human programmed death-1 (PD-1) and its programmed death ligand 1 (PD-L1) protein data bank (PDB) ID: 4ZQK was downloaded from the PDB. The obtained activated CD8+ T-cells propagated well under GE incubation. GE did not interfere with the viability and morphology of activated T-cells at concentrations up to 200 μg/ml and has a weak cytotoxic potential for MDA-MB cells, but, when combined with lymphocyte T-cells, it provides an immunopotentiation effect on MDA-MB-231 breast cancer cells. GE has the strongest binding affinity to PD-1 and PD-L1 to induce immunopotentiation effect. This study illustrates a reasonable prospect of GE as a safe immunopotentiation and anticancer agent. © 2021 Iffan Alif et al. This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).