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岩藻依聚糖/紫外线C联合治疗对口腔癌细胞具有优先抗增殖作用,但对正常细胞无此作用。

Fucoidan/UVC Combined Treatment Exerts Preferential Antiproliferation in Oral Cancer Cells but Not Normal Cells.

作者信息

Chuang Ya-Ting, Shiau Jun-Ping, Yen Ching-Yu, Hou Ming-Feng, Jeng Jiiang-Huei, Tang Jen-Yang, Chang Hsueh-Wei

机构信息

Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.

Division of Breast Oncology and Surgery, Department of Surgery, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan.

出版信息

Antioxidants (Basel). 2022 Sep 12;11(9):1797. doi: 10.3390/antiox11091797.

DOI:10.3390/antiox11091797
PMID:36139871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9495684/
Abstract

Combined treatment is a promising anticancer strategy for improving antiproliferation compared with a single treatment but is limited by adverse side effects on normal cells. Fucoidan (FN), a brown-algae-derived polysaccharide safe food ingredient, exhibits preferential function for antiproliferation to oral cancer but not normal cells. Utilizing the preferential antiproliferation, the impacts of FN in regulating ultraviolet C (UVC) irradiation were assessed in oral cancer cells. A combined treatment (UVC/FN) reduced cell viability of oral cancer cells (Ca9-22 and CAL 27) more than single treatments (FN or UVC), i.e., 53.7%/54.6% vs. 71.2%/91.6%, and 89.2%/79.4%, respectively, while the cell viability of UVC/FN treating on non-malignant oral (S-G) was higher than oral cancer cells, ranging from 106.0 to 108.5%. Mechanistically, UVC/FN preferentially generated higher subG1 accumulation and apoptosis-related inductions (annexin V, caspases 3, 8, and 9) in oral cancer cells than single treatments. UVC/FN preferentially generated higher oxidative stress than single treatments, as evidenced by flow cytometry-detecting reactive oxygen species, mitochondrial superoxide, and glutathione. Moreover, UVC/FN preferentially caused more DNA damage (γH2AX and 8-hydroxy-2'-deoxyguanosine) in oral cancer cells than in single treatments. -acetylcysteine pretreatment validated the oxidative stress effects in these UVC/FN-induced changes. Taken together, FN effectively enhances UVC-triggered antiproliferation to oral cancer cells. UVC/FN provides a promising potential for preferential and synergistic antiproliferation in antioral cancer therapy.

摘要

与单一治疗相比,联合治疗是一种很有前景的抗癌策略,可提高抗增殖能力,但受限于对正常细胞的不良副作用。岩藻依聚糖(FN)是一种源自褐藻的多糖安全食品成分,对口腔癌细胞具有优先抗增殖功能,而对正常细胞则无此作用。利用这种优先抗增殖作用,评估了FN在调节口腔癌细胞中紫外线C(UVC)照射方面的影响。联合治疗(UVC/FN)比单一治疗(FN或UVC)更能降低口腔癌细胞(Ca9-22和CAL 27)的细胞活力,即分别为53.7%/54.6%,而单一治疗分别为71.2%/91.6%和89.2%/79.4%,同时UVC/FN处理非恶性口腔细胞(S-G)的细胞活力高于口腔癌细胞,范围在106.0%至108.5%之间。从机制上讲,与单一治疗相比,UVC/FN在口腔癌细胞中优先产生更高的亚G1期积累和凋亡相关诱导(膜联蛋白V、半胱天冬酶3、8和9)。UVC/FN比单一治疗优先产生更高的氧化应激,流式细胞术检测活性氧、线粒体超氧化物和谷胱甘肽证明了这一点。此外,与单一治疗相比,UVC/FN在口腔癌细胞中优先导致更多的DNA损伤(γH2AX和8-羟基-2'-脱氧鸟苷)。N-乙酰半胱氨酸预处理验证了这些UVC/FN诱导变化中的氧化应激作用。综上所述,FN有效地增强了UVC触发的对口腔癌细胞的抗增殖作用。UVC/FN在抗口腔癌治疗中提供了优先和协同抗增殖的有前景潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/13914ae2879c/antioxidants-11-01797-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/b08c9cab5956/antioxidants-11-01797-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/ebdb79cf1405/antioxidants-11-01797-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/bad3290ab8f7/antioxidants-11-01797-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/3e1a14923ee8/antioxidants-11-01797-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/f63dcdcbe32d/antioxidants-11-01797-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/b1185a03cee6/antioxidants-11-01797-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/600ea33b3c70/antioxidants-11-01797-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/13914ae2879c/antioxidants-11-01797-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/b08c9cab5956/antioxidants-11-01797-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/ebdb79cf1405/antioxidants-11-01797-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/bad3290ab8f7/antioxidants-11-01797-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/d96fd3ead0d4/antioxidants-11-01797-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/2abc8976df77/antioxidants-11-01797-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/3e1a14923ee8/antioxidants-11-01797-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/f63dcdcbe32d/antioxidants-11-01797-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/b1185a03cee6/antioxidants-11-01797-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/600ea33b3c70/antioxidants-11-01797-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/18be/9495684/13914ae2879c/antioxidants-11-01797-g010.jpg

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