Overexpression of NCAPG in ovarian cancer is associated with ovarian cancer proliferation and apoptosis via p38 MAPK signaling pathway.
Overexpression of NCAPG in ovarian cancer is associated with ovarian cancer proliferation and apoptosis via p38 MAPK signaling pathway.
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DOI：
10.1186/s13048-022-01030-z
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发表时间：
2022-08-19
影响因子：
4
通讯作者：
中科院分区：
文献类型：
--
作者：
非平滑肌细胞凝聚素I复合物亚基G（NCAPG）是凝聚素复合物亚基的一个成员，在多种肿瘤中显著过表达，并参与肿瘤的发病机制。然而，NCAPG在卵巢癌中的作用仍不清楚。采用GEPIA和KM RT-PCR数据库分析NCAPG在卵巢癌组织中的mRNA表达、总生存期和无病生存期，采用qPCR和免疫组化分析NCAPG在卵巢癌组织和细胞系中的表达水平。利用靶向NCAPG基因的shRNA（sh-NCAPG）敲低OVCAR 3和SKOV 3细胞中NCAPG的表达。采用CCK-8法、集落形成法、transwell侵袭法和流式细胞术检测NCAPG对OC细胞增殖、凋亡和侵袭能力的影响。最后，通过蛋白质印迹法检测NCAPG在卵巢癌中的作用机制。使用GEPIA和KMTR数据库的分析显示，NCAPG在卵巢癌中上调，并与OC患者的生存呈负相关。qPCR和免疫组化分析证实其在卵巢癌组织和细胞中均呈高表达。沉默NCAPG基因可抑制OC细胞的增殖和侵袭，并诱导OC细胞凋亡。此外，流式细胞仪分析显示，NCAPG敲低阻滞细胞周期在G2和S期。此外，我们还发现下调NCAPG可通过激活p38 MAPK信号通路抑制OC细胞的增殖和侵袭。我们的研究结果表明，NCAPG在卵巢癌的发生和发展中发挥重要作用，并暗示NCAPG作为卵巢癌的潜在治疗靶点。
Non-SMC condensin I complex subunit G (NCAPG), a member of the subunit of condensin complex, is significantly overexpressed in various cancers and involved in the pathogenesis of cancers. However, the roles of NCAPG in ovarian cancer remain unclear. The mRNA expression, overall survival, and disease-free survival of NCAPG in ovarian cancer were analyzed by GEPIA and KM plotter database, and the expression levels of NCAPG in OC tissues and cell lines were determined by qPCR and immunohistochemistry analysis. shRNA targeting NCAPG gene (sh-NCAPG) was utilized to knock down NCAPG expression in OVCAR3 and SKOV3 cells. Subsequently, CCK-8 assay, colony formation assay, transwell invasion assay and flow cytometric analysis were performed to detect the effect of NCAPG on OC cell proliferation, apoptosis, and invasion. Finally, western blot assays were performed to detect the mechanism of NCAPG in ovarian cancer. Analysis using GEPIA and KM plotter database showed NCAPG was upregulated in ovarian cancer and negatively associated with the survival of OC patients. qPCR and immunohistochemistry analysis confirmed it was highly expressed in both ovarian cancer tissues and cells. The silencing of NCAPG inhibited OC cell proliferation and invasion, and induced cell apoptosis. Additionally, flow cytometric analysis revealed that NCAPG knockdown arrested the cell cycle at G2 and S phases. Furthermore, we also found that downregulation of NCAPG could suppress OC cell proliferation and invasion via activating the p38 MAPK signaling pathway. Our results suggest that NCAPG exhibits an important role in the development and progression of ovarian cancer and implicates NCAPG as a potential therapeutic target in ovarian cancer.
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GEPIA：用于癌症和正常基因表达谱和交互式分析的网络服务器。
影响因子：
14.9
作者：
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影响因子：
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