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PAF1 敲低通过抑制 FLOT2 介导的 MEK/ERK1/2 通路来减少宫颈癌细胞的增殖、迁移和侵袭。

Knockdown of PAF1 reduces cervical cancer cell proliferation, migration and invasion via retarding FLOT2-mediated MEK/ERK1/2 pathway.

机构信息

Department of Gynecology, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.

出版信息

Cell Adh Migr. 2023 Dec;17(1):1-10. doi: 10.1080/19336918.2023.2260641. Epub 2023 Sep 27.

DOI:10.1080/19336918.2023.2260641
PMID:37754347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10538450/
Abstract

Cervical cancer (CC) is a very usual reproductive malignant tumor in women. RNA polymerase II-associated factor 1 (PAF1) and flotillin-2 (FLOT2) both have been discovered to key participators in cancers' progression. However, the effects of PAF1/FLOT2 axis on CC development have not been probed. In this study, PAF1 and FLOT2 exhibited higher expression, and silencing of PAF1 down-regulated FLOT2 expression in CC. In addition, the regulatory effects of PAF1 suppression on CC progression were reversed after FLOT2 overexpression. Next, inhibition of PAF1 slowed the tumor growth in vivo through modulating FLOT2. Besides, down-regulation of PAF1 reduced FLOT2 expression to retard the MEK/ERK1/2 pathway. In conclusion, knockdown of PAF1 suppressed CC progression via retarding FLOT2-mediated MEK/ERK1/2 pathway. Our findings illustrated that the PAF1/FLOT2 axis may be useful bio-targets for CC treatment.

摘要

宫颈癌(CC)是女性中一种非常常见的生殖系统恶性肿瘤。RNA 聚合酶 II 相关因子 1(PAF1)和浮球素-2(FLOT2)都被发现是癌症进展的关键参与者。然而,PAF1/FLOT2 轴对 CC 发展的影响尚未被探究。在本研究中,PAF1 和 FLOT2 的表达水平升高,沉默 PAF1 可下调 CC 中的 FLOT2 表达。此外,FLOT2 过表达后,PAF1 抑制对 CC 进展的调节作用被逆转。接下来,通过调节 FLOT2,抑制 PAF1 抑制了体内肿瘤的生长。此外,下调 PAF1 降低了 FLOT2 的表达,从而抑制了 MEK/ERK1/2 通路。总之,敲低 PAF1 通过抑制 FLOT2 介导的 MEK/ERK1/2 通路来抑制 CC 的进展。我们的研究结果表明,PAF1/FLOT2 轴可能是治疗 CC 的有用生物靶标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/fba38aebad6c/KCAM_A_2260641_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/5c84b0193277/KCAM_A_2260641_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/0fe4ba9319f3/KCAM_A_2260641_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/8f2319d215cd/KCAM_A_2260641_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/158f38494f03/KCAM_A_2260641_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/fba38aebad6c/KCAM_A_2260641_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/5c84b0193277/KCAM_A_2260641_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/0fe4ba9319f3/KCAM_A_2260641_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/8f2319d215cd/KCAM_A_2260641_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/158f38494f03/KCAM_A_2260641_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e815/10538450/fba38aebad6c/KCAM_A_2260641_F0005_OC.jpg

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