miR-30a targets STOX2 to increase cell proliferation and metastasis in hydatidiform moles via ERK, AKT, and P38 signaling pathways.
miR-30a targets STOX2 to increase cell proliferation and metastasis in hydatidiform moles via ERK, AKT, and P38 signaling pathways.
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miR-30a 靶向 STOX2 通过 ERK、AKT 和 P38 信号通路增加葡萄胎的细胞增殖和转移
DOI：
10.1186/s12935-022-02503-3
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发表时间：
2022-03-04
影响因子：
5.8
通讯作者：
Sui L
中科院分区：
文献类型：
--
作者：
Guo Z;Zhu C;Wang Y;Li Z;Wang L;Fan J;Xu Y;Zou N;Kong Y;Li D;Sui L
葡萄胎是一种由滋养层细胞异常增殖引起的疾病。microRNA miR-30 a在大多数肿瘤中作为肿瘤抑制基因，参与各种癌症的发展。然而，其在葡萄胎中的作用尚不清楚。采用实时定量逆转录PCR方法检测miR-30 a和STOX 2（编码鹳头盒2）的表达水平。流式细胞术检测miR-30 a和STOX 2表达水平对细胞周期的影响。采用细胞周期试剂盒（Cell Cycle Kit-8）、5-乙炔基-2 ′-脱氧尿苷（5-Ethynyl-2′-deoxyuridine）和集落形成实验检测细胞增殖和活力。Transwell法检测细胞的侵袭和迁移。双荧光素酶报告基因检测和蛋白质印迹法被用来研究所涉及的潜在机制。低miR-30 a表达促进滋养层细胞（miR-10a和HTR-8）的增殖、迁移和侵袭。双荧光素酶测定证实STOX 2是miR-30 a的靶点，并抵抗滋养层细胞中上调的miR-30 a的作用。此外，miR-30 a下调STOX 2可激活ERK、AKT和P38信号通路。这些结果揭示了一种新的机制，即miR-30 a/STOX 2激活ERK、AKT和P38导致葡萄胎滋养层细胞过度增殖。在本研究中，我们发现miR-30 a在葡萄胎的发生发展中起重要作用。我们的研究结果表明，miR-30 a可能通过调控STOX 2而促进人滋养层细胞的恶性转化，这进一步加深了我们对miR-30 a调控滋养层细胞恶性转化作用的理解。在线版本包含补充材料，可通过10.1186/s12935-022-02503-3获取。
A hydatidiform mole is a condition caused by abnormal proliferation of trophoblastic cells. MicroRNA miR-30a acts as a tumor suppressor gene in most tumors and participates in the development of various cancers. However, its role in hydatidiform moles is not clear. Quantitative real-time reverse transcription PCR was used to verify the expression level of miR-30a and STOX2 (encoding storkhead box 2). Flow cytometry assays were performed to detect the cell cycle in cell with different expression levels of miR-30a and STOX2. Cell Cycle Kit-8, 5-ethynyl-2′-deoxyuridine, and colony formation assays were used to detect cell proliferation and viability. Transwell assays was used to test cell invasion and migration. Dual-luciferase reporter assays and western blotting were used to investigate the potential mechanisms involved. Low miR-30a expression promoted the proliferation, migration, and invasion of trophoblastic cells (JAR and HTR-8). Dual luciferase assays confirmed that STOX2 is a target of miR-30a and resisted the effect of upregulated miR-30a in trophoblastic cells. In addition, downregulation of STOX2 by miR-30a could activate ERK, AKT, and P38 signaling pathways. These results revealed a new mechanism by which ERK, AKT, and P38 activation by miR-30a/STOX2 results in excessive proliferation of trophoblast cells in the hydatidiform mole. In this study, we found that miR-30a plays an important role in the development of the hydatidiform mole. Our findings indicate that miR-30a might promote the malignant transformation of human trophoblastic cells by regulating STOX2, which strengthens our understanding of the role of miR-30a in regulating trophoblastic cell transformation. The online version contains supplementary material available at 10.1186/s12935-022-02503-3.
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