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壳寡糖会损害胰腺癌细胞的增殖、侵袭和迁移能力。

Chito-oligosaccharide impairs the proliferation, invasion and migration of pancreatic cancer cells.

作者信息

Liu Han, Ding Siyuan, Lyu Weiyan, Lu Shengyan, Liu Xu

机构信息

Department of Gastroenterology, General Hospital of Northern Theatre Command, 83 Wenhua Road, Shenyang, 110840, Liaoning, China.

出版信息

Discov Oncol. 2025 Mar 12;16(1):298. doi: 10.1007/s12672-025-02015-2.

Abstract

BACKGROUND

Chito-oligosaccharide (COS) is a low molecular weight polymer obtained by degrading chitosan through special enzymatic technology, with good water solubility and high biological activity. It is also the only positively charged cationic basic amino oligosaccharide in nature. Studies have confirmed that COS has antitumour effect, but research on its effect on pancreatic cancer (PC) remains limited and unclear. This study aimed to explore the effects of COS on PC cells (PANC-1 and MIAPaCa-2).

METHOD

We used different concentrations of COS to treat PC cells and conducted Cell Counting Kit-8, wound-healing, and transwell assays to evaluate the proliferation, invasion, and migration ability of PC cells, respectively. Western blot was conducted to assess the expression levels of epithelial-mesenchymal transition (EMT) related markers.

RESULT

The proliferation, invasion, and migration ability of PC cells (PANC-1 and MIAPaCa-2) gradually decreased in a manner dependent on COS concentration. COS at 10 mg/mL exerted the strongest inhibitory effect on the two PC cell lines. At 10 mg/mL, the proliferative activity was 60.61% ± 5.25% and 64.02% ± 4.96%, respectively; the invasive ability was (18.67 ± 4.416) and (31.33 ± 3.162), respectively; and the cell-migration ability was 26.83% ± 0.442% and 17.66% ± 0.647%, respectively. The expression levels of N-cadherin and vimentin were significantly downregulated in PANC-1 cells (0.198 ± 0.047 and 0.225 ± 0.038, respectively) and MIAPaCa-2 cells (0.214 ± 0.094 and 0.214 ± 0.094, respectively) at 10 mg/mL, respectively. Conversely, E-cadherin was upregulated (0.460 ± 0.037 and 0.491 ± 0.047, respectively). Compared with control group, the differences were statistically significant.

CONCLUSION

The upregulation of E-cadherin and the downregulation of vimentin and N-cadherin suggested that the specific mechanism of COS in PC may be related to EMT. This study provided a new direction for PC treatment.

摘要

背景

壳寡糖(COS)是通过特殊酶技术降解壳聚糖得到的低分子量聚合物,具有良好的水溶性和高生物活性。它也是自然界中唯一带正电荷的阳离子碱性氨基寡糖。研究证实COS具有抗肿瘤作用,但关于其对胰腺癌(PC)作用的研究仍然有限且不明确。本研究旨在探讨COS对PC细胞(PANC-1和MIAPaCa-2)的影响。

方法

我们用不同浓度的COS处理PC细胞,并分别进行细胞计数试剂盒-8、伤口愈合和Transwell实验,以评估PC细胞的增殖、侵袭和迁移能力。进行蛋白质免疫印迹法以评估上皮-间质转化(EMT)相关标志物的表达水平。

结果

PC细胞(PANC-1和MIAPaCa-2)的增殖、侵袭和迁移能力以依赖于COS浓度的方式逐渐降低。10mg/mL的COS对两种PC细胞系发挥最强的抑制作用。在10mg/mL时,增殖活性分别为60.61%±5.25%和64.02%±4.96%;侵袭能力分别为(18.67±4.416)和(31.33±3.162);细胞迁移能力分别为26.83%±0.442%和17.66%±0.647%。在10mg/mL时,PANC-1细胞(分别为0.198±0.047和0.225±0.038)和MIAPaCa-2细胞(分别为0.214±0.094和0.214±0.094)中N-钙黏蛋白和波形蛋白的表达水平显著下调。相反,E-钙黏蛋白上调(分别为0.460±0.037和0.491±0.047)。与对照组相比,差异具有统计学意义。

结论

E-钙黏蛋白的上调以及波形蛋白和N-钙黏蛋白的下调表明COS在PC中的具体机制可能与EMT有关。本研究为PC治疗提供了新方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfa9/11896950/3cb203699515/12672_2025_2015_Fig1_HTML.jpg

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