PDF(Pubmed)
Abstract：
UNASSIGNED: To analyze the effect of allicin on the immunoreactivity of osteosarcoma (OS) cells and further explore whether its mechanism is related to the long non-coding Ribonucleic Acid (lncRNA) CBR3-AS1/miR-145-5p/GRP78 axis, so as to provide clinical evidence.
UNASSIGNED: The human OS cell line Saos-2 was treated with allicin at 25, 50, and 100 μmol/L, respectively, to observe changes in cell biological behaviors. Subsequently, CBR3-AS1 abnormal expression vectors were constructed and transfected into Saos-2 to discuss their influence on OS. Furthermore, the regulatory relationship between allicin and the CBR3-AS1/miR-145-5p/GRP78 axis was validated by rescue experiments. Finally, a nude mice tumorigenesis experiment was carried out to analyze the effects of allicin and CBR3-AS1/miR-145-5p/GRP78 axis on the growth of living tumors. Alterations in T-lymphocyte subsets were also detected to assess the effect of allicin on OS immunoreactivity.
UNASSIGNED: With the increase of allicin concentration, Saos-2 activity decreased and apoptosis increased (P < 0.05). In addition, the expression of CBR3-AS1 and GRP78 decreased after allicin intervention, while miR-145-5p increased (P < 0.05). Silencing CBR3-AS1 led to reduced Saos-2 activity, enhanced apoptosis, and activated mitophagy and endoplasmic reticulum stress (P < 0.05). In the rescue experiment, the effect of CBR3-AS1 on OS cells was reversed by silencing miR-145-5p, while the impact of miR-145-5p was reversed by GRP78. Finally, the tumorigenesis experiment in nude mice confirmed the regulatory effects of allicin and CBR3-AS1/miR-145-5p/GRP78 on tumor growth in vivo. Meanwhile, it was seen that allicin activated CD4+CD8+ in OS mice, confirming that allicin has the effect of activating OS immunoreactivity.
UNASSIGNED: Allicin activates OS immunoreactivity and induces apoptosis through the CBR3-AS1/miR-145-5p/GRP78 molecular axis.
UNASSIGNED: The human OS cell line Saos-2 was treated with allicin at 25, 50, and 100 μmol/L, respectively, to observe changes in cell biological behaviors. Subsequently, CBR3-AS1 abnormal expression vectors were constructed and transfected into Saos-2 to discuss their influence on OS. Furthermore, the regulatory relationship between allicin and the CBR3-AS1/miR-145-5p/GRP78 axis was validated by rescue experiments. Finally, a nude mice tumorigenesis experiment was carried out to analyze the effects of allicin and CBR3-AS1/miR-145-5p/GRP78 axis on the growth of living tumors. Alterations in T-lymphocyte subsets were also detected to assess the effect of allicin on OS immunoreactivity.
UNASSIGNED: With the increase of allicin concentration, Saos-2 activity decreased and apoptosis increased (P < 0.05). In addition, the expression of CBR3-AS1 and GRP78 decreased after allicin intervention, while miR-145-5p increased (P < 0.05). Silencing CBR3-AS1 led to reduced Saos-2 activity, enhanced apoptosis, and activated mitophagy and endoplasmic reticulum stress (P < 0.05). In the rescue experiment, the effect of CBR3-AS1 on OS cells was reversed by silencing miR-145-5p, while the impact of miR-145-5p was reversed by GRP78. Finally, the tumorigenesis experiment in nude mice confirmed the regulatory effects of allicin and CBR3-AS1/miR-145-5p/GRP78 on tumor growth in vivo. Meanwhile, it was seen that allicin activated CD4+CD8+ in OS mice, confirming that allicin has the effect of activating OS immunoreactivity.
UNASSIGNED: Allicin activates OS immunoreactivity and induces apoptosis through the CBR3-AS1/miR-145-5p/GRP78 molecular axis.
摘要：
■分析大蒜素对骨肉瘤（OS）细胞免疫反应性的影响，进一步探讨其机制是否与长链非编码核糖核酸（lncRNA）CBR3-AS1/miR-145-5p/GRP78轴有关，从而提供临床证据。
■用25、50和100μmol/L的大蒜素处理人OS细胞系Saos-2，分别,观察细胞生物学行为的变化。随后，构建CBR3-AS1异常表达载体并转染Saos-2,商量其对OS的影响。此外，大蒜素与CBR3-AS1/miR-145-5p/GRP78轴之间的调节关系通过拯救实验得到验证.最后,进行了裸鼠肿瘤发生实验,以分析大蒜素和CBR3-AS1/miR-145-5p/GRP78轴对活体肿瘤生长的影响.还检测了T淋巴细胞亚群的变化以评估大蒜素对OS免疫反应性的影响。
■随着大蒜素浓度的增加，Saos-2活性降低,细胞凋亡增加(P<0.05)。此外,大蒜素干预后，CBR3-AS1和GRP78的表达降低，miR-145-5p升高(P<0.05)。沉默CBR3-AS1导致Saos-2活性降低，细胞凋亡增强，并激活线粒体自噬和内质网应激(P<0.05)。在救援实验中，通过沉默miR-145-5p逆转CBR3-AS1对OS细胞的影响，而miR-145-5p的影响被GRP78逆转。最后,裸鼠肿瘤发生实验证实了大蒜素和CBR3-AS1/miR-145-5p/GRP78对体内肿瘤生长的调节作用。同时,可见大蒜素激活OS小鼠的CD4+CD8+，确认大蒜素具有激活OS免疫反应性的作用。
■大蒜素通过CBR3-AS1/miR-145-5p/GRP78分子轴激活OS免疫反应性并诱导细胞凋亡。
■用25、50和100μmol/L的大蒜素处理人OS细胞系Saos-2，分别,观察细胞生物学行为的变化。随后，构建CBR3-AS1异常表达载体并转染Saos-2,商量其对OS的影响。此外，大蒜素与CBR3-AS1/miR-145-5p/GRP78轴之间的调节关系通过拯救实验得到验证.最后,进行了裸鼠肿瘤发生实验,以分析大蒜素和CBR3-AS1/miR-145-5p/GRP78轴对活体肿瘤生长的影响.还检测了T淋巴细胞亚群的变化以评估大蒜素对OS免疫反应性的影响。
■随着大蒜素浓度的增加，Saos-2活性降低,细胞凋亡增加(P<0.05)。此外,大蒜素干预后，CBR3-AS1和GRP78的表达降低，miR-145-5p升高(P<0.05)。沉默CBR3-AS1导致Saos-2活性降低，细胞凋亡增强，并激活线粒体自噬和内质网应激(P<0.05)。在救援实验中，通过沉默miR-145-5p逆转CBR3-AS1对OS细胞的影响，而miR-145-5p的影响被GRP78逆转。最后,裸鼠肿瘤发生实验证实了大蒜素和CBR3-AS1/miR-145-5p/GRP78对体内肿瘤生长的调节作用。同时,可见大蒜素激活OS小鼠的CD4+CD8+，确认大蒜素具有激活OS免疫反应性的作用。
■大蒜素通过CBR3-AS1/miR-145-5p/GRP78分子轴激活OS免疫反应性并诱导细胞凋亡。
