Wang Lin, Zhang Jinqiu, Sun Angang, Yin Yongxiang, Shen Ye, Zhang Dengxin, Chen Qi, Zhao Min
Department of Gynaecology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China; Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Department of Pathology, Wuxi Maternity and Child Health Care Hospital, Wuxi School of Medicine, Jiangnan University, Wuxi, China.
Placenta. 2024 Dec;158:223-230. doi: 10.1016/j.placenta.2024.10.069. Epub 2024 Nov 2.
Cervical cancer is a leading cause of death in developing countries. Although the placenta is a tumor-like organ, the placental development, including invasive function, is well controlled. One mechanism is that extracellular vesicles (EVs) released from the placenta contribute to this regulation. Placental EVs carry functional proteins and regulatory RNAs. Our previous study reported that placental EVs inhibited ovarian cancer growth in vitro and in vivo.
Whether the inhibitory effect induced by placental EVs also applies to cervical cancer, a non-endocrine-related cancer, in this study, we first co-cultured the cervical tumour tissues with placental explants.
Co-culturing cervical tumour tissues (n = 7) with placental explants showed necrotic signs and increased levels of senescence-associated proteins and death-associated miRNAs, including miRNA-143-3p, miRNA-519a-5p and miRNA-199a-3p in tumour tissues. Additionally, treatment of HeLa cells with placental EVs reduced the viability of HeLa cells and inhibited the ability of invasion and migration of HeLa cells. Increased levels of senescence-associated proteins and reduced levels of proliferative proteins may contribute to the inhibitory effects in HeLa cells.
placental EVs are involved in regulating placental development, and the delivery of cargo significantly impacts the functions of target cells. This study found that factors released from placental explants, likely placental EVs, had anti-tumour effects on the cervical tumour by inhibiting cervical cancer cell viability, invasion, and migration. Cargo in placental EVs, such as cellular death-associated miRNAs, may contribute to the inhibitory effects on cervical tumour.
宫颈癌是发展中国家主要的死亡原因之一。尽管胎盘是一个类似肿瘤的器官，但其发育，包括侵袭功能，受到良好的控制。一种机制是胎盘释放的细胞外囊泡（EVs）有助于这种调节。胎盘EVs携带功能性蛋白质和调节性RNA。我们之前的研究报道胎盘EVs在体外和体内均能抑制卵巢癌的生长。
在本研究中，胎盘EVs诱导的抑制作用是否也适用于宫颈癌这种非内分泌相关癌症，我们首先将宫颈肿瘤组织与胎盘外植体进行共培养。
将宫颈肿瘤组织（n = 7）与胎盘外植体共培养显示出坏死迹象，肿瘤组织中衰老相关蛋白和死亡相关miRNA水平升高，包括miRNA - 143 - 3p、miRNA - 519a - 5p和miRNA - 199a - 3p。此外，用胎盘EVs处理HeLa细胞可降低HeLa细胞的活力，并抑制HeLa细胞的侵袭和迁移能力。衰老相关蛋白水平升高和增殖蛋白水平降低可能导致对HeLa细胞的抑制作用。
胎盘EVs参与调节胎盘发育，其携带的物质传递对靶细胞的功能有显著影响。本研究发现，胎盘外植体释放的因子，可能是胎盘EVs，通过抑制宫颈癌细胞的活力、侵袭和迁移，对宫颈肿瘤具有抗肿瘤作用。胎盘EVs中的物质，如细胞死亡相关的miRNA，可能有助于对宫颈肿瘤的抑制作用。
