RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Role of beta-(1→3)(1→6)-D-glucan derived from yeast on natural killer (NK) cells and breast cancer cell lines in 2D and 3D cultures.
Role of beta-(1→3)(1→6)-D-glucan derived from yeast on natural killer (NK) cells and breast cancer cell lines in 2D and 3D cultures.
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酵母来源的β-(1, 3)(1, 6)-D-葡聚糖可通过增强 NK 细胞免疫反应以及抑制乳腺癌细胞生长,有助于癌症的治疗。
β-(1,3)(1,6)-D-葡聚糖是一种复杂多糖,存在于多种真菌、酵母、细菌、藻类、大麦和燕麦的细胞壁中,具有免疫调节、抗癌和抗病毒作用。在本研究中,我们探讨了来源于酵母的β-(1,3)(1,6)-D-葡聚糖对原代NK细胞和乳腺癌细胞系在2D和3D模型中增殖的影响,以及对原代NK细胞在2D和3D模型中对乳腺癌细胞系细胞毒性的影响。
在本研究中,我们使用XTT细胞增殖 assay 和CellTiter-Glo 2.0 assay,在2D和3D模型中研究了不同浓度的酵母来源β-(1 3)(1 6)-D-葡聚糖对人NK细胞增殖和细胞毒性以及乳腺癌细胞系的影响,以确定人NK细胞在2D和3D模型中对乳腺癌细胞系的细胞毒性。
我们发现,在无IL2条件下将NK细胞与β-葡聚糖共孵育48小时可显著增加NK细胞的增殖,而在有IL2(70 U/ml)条件下将NK细胞与β-葡聚糖共孵育虽增加NK细胞增殖但不显著。此外,β-葡聚糖在2D模型中显著抑制乳腺癌细胞系的增殖,并对乳腺癌多细胞肿瘤球体(3D)诱导了微弱且不显著的生长抑制效应。另外,在2D和3D模型中检测了NK细胞对乳腺癌细胞系的细胞毒性,β-葡聚糖显著增加了NK细胞对MCF-7(2D中)的细胞毒性。
Beta-(1,3)(1,6)-D-glucan is a complex polysaccharide, which is found in the cell wall of various fungi, yeasts, bacteria, algae, barley, and oats and has immunomodulatory, anticancer and antiviral effects. In the present study, we investigated the effect of beta-(1,3)(1,6)-D-glucan derived from yeast on the proliferation of primary NK cells and breast cancer cell lines in 2D and 3D models, and on the cytotoxicity of primary NK cells against breast cancer cell lines in 2D and 3D models.
In this study, we investigated the effects of different concentrations of yeast-derived beta-(1 3)(1 6)-D-glucan on the proliferation and cytotoxicity of human NK cells and breast cancer cell lines in 2D and 3D models using the XTT cell proliferation assay and the CellTiter-Glo 2.0 assay to determine the cytotoxicity of human NK cells on breast cancer cell lines in 2D and 3D models.
We found that the co-incubation of NK cells with beta-glucan in the absence of IL2 at 48 h significantly increased the proliferation of NK cells, whereas the co-incubation of NK cells with beta-glucan in the presence of IL2 (70 U/ml) increased the proliferation of NK cells but not significantly. Moreover, beta-glucan significantly inhibited the proliferation of breast cancer cell lines in 2D model and induced a weak, non-significant growth inhibitory effect on breast cancer multicellular tumor spheroids (3D). In addition, the cytotoxicity of NK cells against breast cancer cell lines was examined in 2D and 3D models, and beta-glucan significantly increased the cytotoxicity of NK cells against MCF-7 (in 2D).
Yeast derived beta-(1,3)(1,6)-D-glucan could contribute to the treatment of cancer by enhancing NK cell immune response as well as contributing to inhibition of breast cancer cell growth.
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