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RAB11A通过激活FAK/AKT信号通路促进前列腺癌的细胞恶性进展和肿瘤形成。

RAB11A Promotes Cell Malignant Progression and Tumor Formation of Prostate Cancer via Activating FAK/AKT Signaling Pathway.

作者信息

Chen Weifang, Wang Junjun

机构信息

Department of Hematology Oncology, Zhejiang Putuo Hospital, Zhoushan 316100, China.

Department of Urology, Xiaoshan First Affiliated Hospital of Hangzhou Normal University, Hangzhou 311200, China.

出版信息

Evid Based Complement Alternat Med. 2023 Jan 31;2023:5885387. doi: 10.1155/2023/5885387. eCollection 2023.

DOI:10.1155/2023/5885387
PMID:36760469
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9904921/
Abstract

BACKGROUND

RAB11A, a member of the GTPase family, acts as a regulator in diverse cancers development. The dysregulation of the FAK/AKT signaling pathway is mainly related to tumorigenesis. This study aimed to investigate the possible effect of RAB11A in prostate cancer and further explore the potential mechanisms.

RESULTS

In this study, we illustrated the tumor-promoting effects of RAB11A based on and experiments. RAB11A expression was upregulated in prostate cancer cells. RAB11A knockdown decreased the prostate cancer cell proliferation, migration, and invasion. RAB11A also induced the epithelial-mesenchymal transition. PF562271 suppressed the malignant characteristics of prostate cancer cells caused by RAB11A knockdown. Furthermore, the interference of RAB11A reduced the tumor growth and the protein levels of p-FAK/FAK and p-AKT/AKT .

CONCLUSION

RAB11A promotes cell malignant progression and tumor formation in prostate cancer via activating FAK/AKT signaling pathway.

摘要

背景

RAB11A是小GTP酶家族的成员之一，在多种癌症发展过程中发挥调节作用。黏着斑激酶（FAK）/蛋白激酶B（AKT）信号通路失调主要与肿瘤发生相关。本研究旨在探究RAB11A在前列腺癌中的可能作用，并进一步探索其潜在机制。

结果

在本研究中，我们通过[具体实验1]和[具体实验2]实验证明了RAB11A具有促肿瘤作用。前列腺癌细胞中RAB11A表达上调。敲低RAB11A可降低前列腺癌细胞的增殖、迁移和侵袭能力。RAB11A还可诱导上皮-间质转化。PF562271可抑制敲低RAB11A所导致的前列腺癌细胞的恶性特征。此外，干扰RAB11A可减少肿瘤生长，并降低磷酸化FAK/FAK和磷酸化AKT/AKT的蛋白水平。

结论

RAB11A通过激活FAK/AKT信号通路促进前列腺癌细胞的恶性进展和肿瘤形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/81966cb5e827/ECAM2023-5885387.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/9835b3062681/ECAM2023-5885387.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/ee31232fa8e6/ECAM2023-5885387.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/7fbe248b39aa/ECAM2023-5885387.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/217f9ef2cf68/ECAM2023-5885387.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/85ac052f773b/ECAM2023-5885387.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/81966cb5e827/ECAM2023-5885387.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/9835b3062681/ECAM2023-5885387.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/ee31232fa8e6/ECAM2023-5885387.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/7fbe248b39aa/ECAM2023-5885387.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/217f9ef2cf68/ECAM2023-5885387.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/85ac052f773b/ECAM2023-5885387.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2447/9904921/81966cb5e827/ECAM2023-5885387.006.jpg

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