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纤维连接蛋白 3 敲低抑制宫颈癌在体内外的生长和转移。

Fibulin-3 knockdown inhibits cervical cancer cell growth and metastasis in vitro and in vivo.

机构信息

Department of Obstetrics and Gynecology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, 250021, China.

Department of Obstetrics and Gynecology, Shan Xian Maternal and Child Care and family planning service center, Shan Xian, 274300, China.

出版信息

Sci Rep. 2018 Jul 13;8(1):10594. doi: 10.1038/s41598-018-28906-9.

DOI:10.1038/s41598-018-28906-9
PMID:30006571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6045626/
Abstract

To explore the function of fibulin-3 in cervical carcinoma malignant cell growth and metastasis, fibulin-3 expression in normal cervical tissue, cervical intraepithelial neoplasia (CIN), and cervical carcinoma were evaluated by immunohistochemistry. Quantitative real-time-polymerase chain reaction, western blotting, and immunocytochemistry were performed to assess the expression of fibulin-3 at mRNA and protein levels in different invasive clone sublines. Fibulin-3 shRNA and fibulin-3 cDNA were used to transfect the strongly and weakly invasive clone sublines. Using in vitro and in vivo functional assays, we investigated the effects of down-regulating and up-regulating fibulin-3 expression on the proliferation and invasion of different clone sublines. Epithelial mesenchymal transition (EMT) and its signaling pathways PI3K/AKT and ERK were studied carefully in lentiviral transfection systems. Fibulin-3 was upregulated in cervical carcinoma, and its overexpression was significantly related with malignant phenotype and poor prognosis of cervical carcinoma. Fibulin-3 promoted cervical cancer cell invasive capabilities by eliciting EMT and activating the PI3K-Akt-mTOR signal transduction pathway. Fibulin-3 could facilitate the process of cervical cancer development. The results presented here will help develop novel prognostic factors and possible therapeutic options for patients with cervical cancer.

摘要

为了探究纤连蛋白 3 在宫颈癌恶性细胞生长和转移中的作用，本研究通过免疫组织化学方法评估了纤连蛋白 3 在正常宫颈组织、宫颈上皮内瘤变（CIN）和宫颈癌中的表达。通过实时定量聚合酶链反应、western blot 和免疫细胞化学方法，评估了不同侵袭性克隆亚系中纤连蛋白 3 在 mRNA 和蛋白水平的表达。使用纤连蛋白 3 shRNA 和纤连蛋白 3 cDNA 转染强侵袭性和弱侵袭性克隆亚系。通过体外和体内功能实验，研究了下调和上调纤连蛋白 3 表达对不同克隆亚系增殖和侵袭能力的影响。在慢病毒转染系统中，仔细研究了上皮间质转化（EMT）及其信号通路 PI3K/AKT 和 ERK。纤连蛋白 3 在宫颈癌中上调，其过表达与宫颈癌的恶性表型和不良预后显著相关。纤连蛋白 3 通过引发 EMT 并激活 PI3K-Akt-mTOR 信号转导通路，促进宫颈癌细胞的侵袭能力。纤连蛋白 3 可能促进宫颈癌的发展。本研究结果将有助于为宫颈癌患者开发新的预后因素和可能的治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/76cd7332e194/41598_2018_28906_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/0c6d1db3b2cd/41598_2018_28906_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/7ec0d880ada6/41598_2018_28906_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/80e9a2bb608c/41598_2018_28906_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/45cda9d575cd/41598_2018_28906_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/88515035a099/41598_2018_28906_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/fabd392f8308/41598_2018_28906_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/39325222d1fc/41598_2018_28906_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/c4bdea20adf9/41598_2018_28906_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/59828496bb93/41598_2018_28906_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/22ba062b8042/41598_2018_28906_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/2c0e2d635fc3/41598_2018_28906_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/76cd7332e194/41598_2018_28906_Fig12_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/0c6d1db3b2cd/41598_2018_28906_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/7ec0d880ada6/41598_2018_28906_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/80e9a2bb608c/41598_2018_28906_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/45cda9d575cd/41598_2018_28906_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/88515035a099/41598_2018_28906_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/fabd392f8308/41598_2018_28906_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/39325222d1fc/41598_2018_28906_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/c4bdea20adf9/41598_2018_28906_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/59828496bb93/41598_2018_28906_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/22ba062b8042/41598_2018_28906_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/2c0e2d635fc3/41598_2018_28906_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6e58/6045626/76cd7332e194/41598_2018_28906_Fig12_HTML.jpg

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