高产乳酸是各种肿瘤的常见特征。乳酸是一种免疫抑制分子，对于肿瘤细胞的免疫逃逸具有至关重要的作用，这很大程度上归因于其对于肿瘤微环境(TME)中存在的T细胞的负面影响。降低肿瘤细胞的糖酵解速率的策略可以增强免疫监视并限制肿瘤生长。丙酮酸激酶M2 (PKM2) 是糖酵解途径中的关键酶，它对TME中乳酸积累具有重要作用。微小RNA(miR)-124已被证明可以通过降低PKM2水平间接减少肿瘤细胞乳酸合成。在这项研究中，我们首先在肿瘤细胞中过表达miR-124，使用实时荧光定量PCR(qRT-PCR)和分光光度法评估其对肿瘤细胞PKM2表达和乳酸产生的影响。然后，我们将miR-124处理的肿瘤细胞与T细胞共培养，以研究miR-124过表达对T细胞增殖、细胞因子产生和凋亡的影响。我们的结果表明，通过调节肿瘤细胞的葡萄糖代谢，miR-124过表达可以显著减少肿瘤细胞产生的乳酸量，从而增强T细胞的增殖和干扰素-γ产生。此外，它可以挽救T细胞免受乳酸诱导的凋亡。我们的数据表明，乳酸是T细胞免疫治疗的一个阻碍因素，然而，通过miR-124调节肿瘤细胞的代谢途径，可以是提高T细胞的抗肿瘤反应的一种有前途的途径。

High production of lactic acid is a common feature of various tumors. Lactic acid is an immunosuppressive molecule with crucial roles in tumor cells' immune escape, which could largely be attributed to its negative effects on the T cells present in the tumor microenvironment (TME). Strategies that decrease the glycolysis rate of tumor cells could enhance immunosurveillance and limit tumor growth. Pyruvate kinase M2 (PKM2) is a key enzyme in the glycolysis pathway, and it plays a vital role in lactic acid buildup in the TME. MicroRNA (miR)-124 has been shown to be able to decrease tumor cell lactic acid synthesis indirectly by reducing PKM2 levels. In this study, we first overexpressed miR-124 in the tumor cells and evaluated its effects on the PKM2 expression and lactic acid production of the tumor cells using quantitative real-time polymerase chain reaction (qRT-PCR) and spectrophotometry, respectively. Then, we cocultured miR-124-treated tumor cells with T cells to investigate the effects of miR-124 overexpression on T cell proliferation, cytokine production, and apoptosis. Our results demonstrated that miR-124 overexpression could significantly reduce the amount of lactic acid produced by tumor cells by manipulating their glucose metabolism, which led to the augmented proliferation and IFN-γ production of T cells. Moreover, it rescued T cells from lactic acid-induced apoptosis. Our data suggest that lactic acid is a hindering factor for T-cell-based immunotherapies; however, manipulating tumor cells' metabolism via miR-124 could be a promising way to improve antitumor responses of T cells.