Tomoyo Agura, Seulgi Shin, Hyejung Jo, Seoyoun Jeong, Hyovin Ahn, So Young Pang, June Lee, Jeong-Ho Park, Yejin Kim, Jae Seung Kang
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CD69, a marker known for activating for NK cells, which had decreased due to vitamin C deficiency, did not recover with vitamin C treatment but showed an increasing with Aptamin C. Furthermore, the expression of CD107a, a cell surface marker that increases during the killing process of target cells, also did not recover with vitamin C but increased with Aptamin C. Based on these results, when cultured with tumor cells to measure the extent of tumor cell death, an increase in tumor cell death was observed. To investigate the signaling mechanisms and related molecules involved in the proliferation and activation of NK cells by Aptamin C showed that Aptamin C treatment led to an increase in intracellular STAT3 activation. In conclusion, Aptamin C has a higher capability to activate NK cells and induce tumor cell death compared to vitamin C and it is mediated through the activation of STAT3.</p>","PeriodicalId":7831,"journal":{"name":"Anatomy & Cell Biology","volume":" ","pages":"408-418"},"PeriodicalIF":1.4000,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424563/pdf/","citationCount":"0","resultStr":"{\"title\":\"Aptamin C enhances anti-cancer activity NK cells through the activation of STAT3: a comparative study with vitamin C.\",\"authors\":\"Tomoyo Agura, Seulgi Shin, Hyejung Jo, Seoyoun Jeong, Hyovin Ahn, So Young Pang, June Lee, Jeong-Ho Park, Yejin Kim, Jae Seung Kang\",\"doi\":\"10.5115/acb.24.120\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Vitamin C is a well-known antioxidant with antiviral, anticancer, and anti-inflammatory properties based on its antioxidative function. Aptamin C, a complex of vitamin C with its specific aptamer, has been reported to maintain or even enhance the efficacy of vitamin C while increasing its stability. To investigate <i>in vivo</i> distribution of Aptamin C, Gulo knockout mice, which, like humans, cannot biosynthesize vitamin C, were administered Aptamin C orally for 2 and 4 weeks. The results showed higher vitamin C accumulation in all tissues when administered Aptamin C, especially in the spleen. Next, the activity of natural killer (NK) cells were conducted. CD69, a marker known for activating for NK cells, which had decreased due to vitamin C deficiency, did not recover with vitamin C treatment but showed an increasing with Aptamin C. Furthermore, the expression of CD107a, a cell surface marker that increases during the killing process of target cells, also did not recover with vitamin C but increased with Aptamin C. Based on these results, when cultured with tumor cells to measure the extent of tumor cell death, an increase in tumor cell death was observed. To investigate the signaling mechanisms and related molecules involved in the proliferation and activation of NK cells by Aptamin C showed that Aptamin C treatment led to an increase in intracellular STAT3 activation. 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引用次数: 0
摘要
维生素 C 是一种众所周知的抗氧化剂,具有抗病毒、抗癌和消炎的作用。Aptamin C是维生素C与其特异性适配体的复合物,有报道称它能保持甚至增强维生素C的功效,同时提高其稳定性。为了研究 Aptamin C 在体内的分布情况,我们给 Gulo 基因敲除小鼠口服了 2 周和 4 周 Aptamin C。结果表明,给小鼠口服七叶皂苷 C 后,维生素 C 在所有组织中的蓄积量都增加了,尤其是在脾脏中。接下来,研究人员对自然杀伤(NK)细胞的活性进行了检测。此外,在杀死靶细胞过程中会增加的细胞表面标志物 CD107a 的表达也没有随着维生素 C 的服用而恢复,但在服用万通维生素 C 后却有所增加。在研究七叶皂苷 C 参与 NK 细胞增殖和激活的信号机制和相关分子时发现,七叶皂苷 C 处理会导致细胞内 STAT3 激活增加。总之,与维生素 C 相比,Aptamin C 激活 NK 细胞和诱导肿瘤细胞死亡的能力更强,而且是通过激活 STAT3 介导的。
Aptamin C enhances anti-cancer activity NK cells through the activation of STAT3: a comparative study with vitamin C.
Vitamin C is a well-known antioxidant with antiviral, anticancer, and anti-inflammatory properties based on its antioxidative function. Aptamin C, a complex of vitamin C with its specific aptamer, has been reported to maintain or even enhance the efficacy of vitamin C while increasing its stability. To investigate in vivo distribution of Aptamin C, Gulo knockout mice, which, like humans, cannot biosynthesize vitamin C, were administered Aptamin C orally for 2 and 4 weeks. The results showed higher vitamin C accumulation in all tissues when administered Aptamin C, especially in the spleen. Next, the activity of natural killer (NK) cells were conducted. CD69, a marker known for activating for NK cells, which had decreased due to vitamin C deficiency, did not recover with vitamin C treatment but showed an increasing with Aptamin C. Furthermore, the expression of CD107a, a cell surface marker that increases during the killing process of target cells, also did not recover with vitamin C but increased with Aptamin C. Based on these results, when cultured with tumor cells to measure the extent of tumor cell death, an increase in tumor cell death was observed. To investigate the signaling mechanisms and related molecules involved in the proliferation and activation of NK cells by Aptamin C showed that Aptamin C treatment led to an increase in intracellular STAT3 activation. In conclusion, Aptamin C has a higher capability to activate NK cells and induce tumor cell death compared to vitamin C and it is mediated through the activation of STAT3.