FNBP1 Facilitates Cervical Cancer Cell Survival by the Constitutive Activation of FAK/PI3K/AKT/mTOR Signaling

作者全名："Zhang, Jun; Li, Xin; Zhou, Yunfei; Lin, Mingming; Zhang, Qianying; Wang, Yunhong"

作者地址："[Zhang, Jun; Li, Xin; Zhou, Yunfei; Lin, Mingming; Zhang, Qianying; Wang, Yunhong] Chongqing Med Univ, Basic Med Sch, Chongqing 400016, Peoples R China"

通信作者："Zhang, J (通讯作者)，Chongqing Med Univ, Basic Med Sch, Chongqing 400016, Peoples R China."

来源：CELLS

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:001045354300001

JCR分区：Q2

影响因子：5.1

年份：2023

卷号：12

期号：15

开始页：　

结束页：　

文献类型：Article

关键词：FNBP1; cervical cancer; cell adhesion; FAK; PI3K; AKT signaling; cell survival

摘要："Cervical cancer is the most prevalent gynecological tumor among women worldwide. Although the incidence and mortality of cervical cancer have been declining thanks to the wide-scale implementation of cytological screening, it remains a major challenge in clinical treatment. High viability is one of the leading causes of the chemotherapeutic resistance in cervical cancers. Formin-binding protein 1 (FNBP1) could stimulate F-actin polymerization beneath the curved plasma membrane in the cell migration and endocytosis, which had previously been well defined. Here, FNBP1 was also demonstrated to play a crucial role in cervical cancer cell survival, and the knockdown of which could result in the attenuation of FAK/PI3K/AKT signaling followed by significant apoptotic accumulation and proliferative inhibition. In addition, the epidermal growth factor (hrEGF) abrogated all the biological effects mediated by the silencing of FNBP1 except for the cell adhesion decrease. These findings indicated that FNBP1 plays a key role in maintaining the activity of focal adhesion kinase (FAK) by promoting cell adhesion. The activated FAK positively regulated downstream PI3K/AKT/mTOR signaling, which is responsible for cell survival. Promisingly, FNBP1 might be a potential target against cervical cancer in combination therapy."

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