Abstract：
This study was aimed to uncover the character and potential regulatory mechanism of EPB41L3 in cervical cancer (CC). CC cells were injected into BALB/c nude mice (female) to construct a xenograft tumor model. Real-time quantitative polymerase chain reaction (qRT-PCR) and western blot were performed to evaluate the expression of EPB41L3, ERK/p38 MAPK signal markers in CC tissues and cells. Cell counting kit-8 (CCK-8) and Transwell was applied to analyze the viability, invasion, and migration of CC cell lines. EPB41L3 was substantially decreased both in CC tissues and cells. Cell viability, invasion, and migration of CC cells were reduced by overexpressing EPB41L3. Bioinformatics analysis prerdicted that EPB41L3 was strongly related to the ERK/p38 MAPK pathway. Compared with Ad-nc mice, the volume and weight of tumors and ERK/p38 MAPK signal markers were down-regulated in Ad-EPB41L3 mice. After knocking down EPB41L3 with EPB41L3 siRNA (siEPB41L3), the ERK/p38 MAPK pathway was activated. Moreover, SB203580 treatment reversed the effect of EPB41L3 silencing on the improvement in viability, migration, and invasion of CC cells. EPB41L3 suppresses the progression of CC via activating the ERK/p38 MAPK pathway. EPB41L3 may serve as an effective therapeutic target for CC.
摘要：
本研究旨在揭示EPB41L3在宫颈癌（CC）中的特征和潜在的调控机制。将CC细胞注射到BALB/c裸鼠(雌性)中以构建异种移植肿瘤模型。采用实时定量聚合酶链反应(qRT-PCR)和Westernblot检测EPB41L3、ERK/p38MAPK信号标记在CC组织和细胞中的表达。应用细胞计数试剂盒-8(CCK-8)和Transwell分析其活力,入侵,和CC细胞系的迁移。EPB41L3在CC组织和细胞中均显著降低。细胞活力，入侵,通过过表达EPB41L3减少CC细胞的迁移。生物信息学分析表明，EPB41L3与ERK/p38MAPK通路密切相关。与Ad-NC小鼠相比，Ad-EPB41L3小鼠的肿瘤体积和重量以及ERK/p38MAPK信号标记物下调。用EPB41L3siRNA（siEPB41L3）敲除EPB41L3后，ERK/p38MAPK通路被激活。此外，SB203580处理逆转了EPB41L3沉默对生存能力提高的影响，迁移,和CC细胞的侵袭。EPB41L3通过激活ERK/p38MAPK通路抑制CC的进展。EPB41L3可作为CC的有效治疗靶标。
