Jagged1 contained in MSC-derived small extracellular vesicles promotes squamous differentiation of cervical cancer by activating NOTCH pathway.

Jagged1 contained in MSC-derived small extracellular vesicles promotes squamous differentiation of cervical cancer by activating NOTCH pathway.
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MSC来源的小细胞外囊泡中含有的Jagged1通过激活NOTCH通路促进宫颈癌的鳞状分化。

DOI:
10.1007/s00432-023-05495-3
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发表时间:
2023-12
影响因子:
3.6
通讯作者:
--
中科院分区:
医学3区
文献类型:
--
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宫颈癌是女性第四大常见癌症,对女性健康构成重大威胁,迫切需要新的治疗方法。本研究首次成功提取并鉴定了人脐带间充质干细胞分泌的细胞外小泡。我们在体外研究了MSC-sEV对宫颈癌CaSki细胞鳞状分化水平的影响,并探讨了MSC-sEV对NOTCH途径、宫颈癌细胞生长、增殖、迁移能力和鳞状分化水平的影响。MSC-sEV的作用也在人角质形成细胞HaCaT细胞中得到验证。结果表明,MSC-sEV上的Jagged 1蛋白可与宫颈癌细胞上的NOTCH 1结合,激活NOTCH信号,促进CaSki细胞的鳞状分化水平,从而抑制CaSki细胞的生长、增殖和迁移能力。MSC-sEV还可以激活HaCaT细胞中的NOTCH通路,但促进HaCaT细胞的活力。MSC-sEV可激活NOTCH通路,促进CaSki细胞向鳞状细胞分化,抑制CaSki细胞的生长、增殖和迁移能力,这可能是其治疗宫颈癌的新机制。在线版本包含补充材料,可通过10.1007/s 00432 -023-05495-3获得。
Cervical cancer is the fourth most common cancer in women and poses a major threat to women's health, urgently requiring new treatment methods. This study first successfully extracted and identified small extracellular vesicles secreted by human umbilical cord-derived mesenchymal stem cells. We studied the effects of MSC-sEV on the squamous differentiation levels of cervical cancer CaSki cells in vitro, and explored the effects of MSC-sEV on the NOTCH pathway, the growth, proliferation, migration abilities and squamous differentiation levels of cervical cancer cells. The roles of MSC-sEV were also verified in human keratinocyte HaCaT cells. The results showed that Jagged1 protein on MSC-sEV can bind to NOTCH1 on cervical cancer cells, activate NOTCH signaling, and promote squamous differentiation levels in CaSki cells, thus inhibiting the growth, proliferation and migration abilities of CaSki cells. MSC-sEV can also activate the NOTCH pathway in HaCaT cells, but promote the viability of HaCaT cells. MSC-sEV can activate the NOTCH pathway to promote squamous differentiation of CaSki cells and inhibit the growth proliferation and migration abilities of CaSki cells which may be a new mechanism for cervical cancer treatment. The online version contains supplementary material available at 10.1007/s00432-023-05495-3.
DOI: 10.1186/1476-4598-12-38
发表时间: 2013-05-07
期刊: Molecular cancer
影响因子: 37.3
作者:
French D;Belleudi F;Mauro MV;Mazzetta F;Raffa S;Fabiano V;Frega A;Torrisi MR
通讯作者: Torrisi MR