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FNBP1 通过组成性激活 FAK/PI3K/AKT/mTOR 信号促进宫颈癌细胞存活。

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

机构信息

Basic Medical School, Chongqing Medical University, Chongqing 400016, China.

出版信息

Cells. 2023 Jul 29;12(15):1964. doi: 10.3390/cells12151964.

DOI:10.3390/cells12151964
PMID:37566043
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10417648/
Abstract

Cervical cancer is the most prevalent 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.

摘要

宫颈癌是全球女性中最常见的癌症。尽管由于细胞学筛查的广泛实施，宫颈癌的发病率和死亡率有所下降，但它仍然是临床治疗中的一个主要挑战。高活力是宫颈癌化疗耐药的主要原因之一。formin 结合蛋白 1 (FNBP1) 可以在细胞迁移和内吞作用中刺激弯曲的质膜下的 F-肌动蛋白聚合，这一点以前已经得到了很好的定义。在这里，FNBP1 也被证明在宫颈癌细胞存活中起着至关重要的作用，其敲低可导致粘着斑激酶 (FAK)/PI3K/AKT 信号的衰减，随后出现明显的凋亡积累和增殖抑制。此外，表皮生长因子 (hrEGF) 除了降低细胞黏附外，还能消除 FNBP1 沉默介导的所有生物学效应。这些发现表明，FNBP1 通过促进细胞黏附在维持粘着斑激酶 (FAK) 的活性方面起着关键作用。激活的 FAK 正向调节下游的 PI3K/AKT/mTOR 信号，该信号负责细胞存活。有希望的是，FNBP1 可能成为联合治疗宫颈癌的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/51697b7184a9/cells-12-01964-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/02e74665b30e/cells-12-01964-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/24001f28b271/cells-12-01964-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/7879787f8fe6/cells-12-01964-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/51697b7184a9/cells-12-01964-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/c0aee8d2449c/cells-12-01964-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/264654d38fec/cells-12-01964-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/a492cce337b2/cells-12-01964-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/6121f07387af/cells-12-01964-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/02e74665b30e/cells-12-01964-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/24001f28b271/cells-12-01964-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/7879787f8fe6/cells-12-01964-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cd34/10417648/51697b7184a9/cells-12-01964-g008.jpg

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