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Abstract：
Ovarian cancer is one of the most fatal malignancies of the female reproductive system. The purpose of this study is to explore the mechanism of Actin Related Protein 2/3 Complex Subunit 1B(ARPC1B) in the progression of ovarian cancer.
The expressions and prognostic value of ARPC1B in ovarian cancer were identified using the GEPIA database and the Kaplan-Meier Plotter database. The expression of ARPC1B was manipulated to evaluate its impact on the malignant phenotypes of ovarian cancer. The cell proliferation ability was analyzed through CCK-8 assay and clone formation assay. The cell migration and invasion capacity was evaluated through wound healing assay and trans well assay. Mice xenografts were conducted to measure the effects of ARPC1B on tumor development in vivo.
Our data suggested that ARPC1B was overexpressed in ovarian cancer, which was correlated with a poorer survival compared to low mRNA expression of ARPC1B in ovarian cancer patients. The overexpression of ARPC1B promoted cell proliferation, migration, and invasion of ovarian cancer cells. Conversely, the knockdown of ARPC1B resulted in the opposite effect. Additionally, ARPC1B expression could activate Wnt/β-catenin signaling pathway. The administration of the β-catenin inhibitor XAV-939 abolished the promotion of cell proliferation, migration, and invasion activities induced by ARPC1B overexpression in vitro.
ARPC1B was overexpressed in ovarian cancer and was correlated with poor prognosis. ARPC1B promoted ovarian cancer progression through activation of Wnt/β-catenin Signaling Pathway.
The expressions and prognostic value of ARPC1B in ovarian cancer were identified using the GEPIA database and the Kaplan-Meier Plotter database. The expression of ARPC1B was manipulated to evaluate its impact on the malignant phenotypes of ovarian cancer. The cell proliferation ability was analyzed through CCK-8 assay and clone formation assay. The cell migration and invasion capacity was evaluated through wound healing assay and trans well assay. Mice xenografts were conducted to measure the effects of ARPC1B on tumor development in vivo.
Our data suggested that ARPC1B was overexpressed in ovarian cancer, which was correlated with a poorer survival compared to low mRNA expression of ARPC1B in ovarian cancer patients. The overexpression of ARPC1B promoted cell proliferation, migration, and invasion of ovarian cancer cells. Conversely, the knockdown of ARPC1B resulted in the opposite effect. Additionally, ARPC1B expression could activate Wnt/β-catenin signaling pathway. The administration of the β-catenin inhibitor XAV-939 abolished the promotion of cell proliferation, migration, and invasion activities induced by ARPC1B overexpression in vitro.
ARPC1B was overexpressed in ovarian cancer and was correlated with poor prognosis. ARPC1B promoted ovarian cancer progression through activation of Wnt/β-catenin Signaling Pathway.
摘要：
■卵巢癌是女性生殖系统最致命的恶性肿瘤之一。目的探讨肌动蛋白相关蛋白2/3复合物亚基1B(ARPC1B)在卵巢癌进展中的作用机制。
■使用GEPIA数据库和Kaplan-Meier绘图仪数据库鉴定ARPC1B在卵巢癌中的表达和预后价值。操纵ARPC1B的表达以评估其对卵巢癌恶性表型的影响。通过CCK-8测定和克隆形成测定分析细胞增殖能力。通过伤口愈合试验和跨孔试验评估细胞迁移和侵袭能力。进行小鼠异种移植物以测量ARPC1B对体内肿瘤发展的影响。
■我们的数据表明ARPC1B在卵巢癌中过度表达，与卵巢癌患者ARPC1B的低mRNA表达相比，这与较低的生存率相关。ARPC1B过表达促进细胞增殖,迁移,和卵巢癌细胞的侵袭。相反，ARPC1B的敲低导致相反的效果.此外,ARPC1B表达可激活Wnt/β-catenin信号通路。β-连环蛋白抑制剂XAV-939的给药取消了细胞增殖的促进，迁移,和体外ARPC1B过表达诱导的侵袭活性。
■ARPC1B在卵巢癌中过度表达，与预后不良相关。ARPC1B通过激活Wnt/β-catenin信号通路促进卵巢癌进展。
■使用GEPIA数据库和Kaplan-Meier绘图仪数据库鉴定ARPC1B在卵巢癌中的表达和预后价值。操纵ARPC1B的表达以评估其对卵巢癌恶性表型的影响。通过CCK-8测定和克隆形成测定分析细胞增殖能力。通过伤口愈合试验和跨孔试验评估细胞迁移和侵袭能力。进行小鼠异种移植物以测量ARPC1B对体内肿瘤发展的影响。
■我们的数据表明ARPC1B在卵巢癌中过度表达，与卵巢癌患者ARPC1B的低mRNA表达相比，这与较低的生存率相关。ARPC1B过表达促进细胞增殖,迁移,和卵巢癌细胞的侵袭。相反，ARPC1B的敲低导致相反的效果.此外,ARPC1B表达可激活Wnt/β-catenin信号通路。β-连环蛋白抑制剂XAV-939的给药取消了细胞增殖的促进，迁移,和体外ARPC1B过表达诱导的侵袭活性。
■ARPC1B在卵巢癌中过度表达，与预后不良相关。ARPC1B通过激活Wnt/β-catenin信号通路促进卵巢癌进展。
