TRIB1 facilitates the proliferation and migration of ovarian cancer cells by inducing EMT progression.

IF 2.5 4区 生物学 Q3 CELL BIOLOGY Histology and histopathology Pub Date : 2024-12-31 DOI:10.14670/HH-18-868
Guangyan Shi, Kristian Holgersson, Zhen Xin, Laszlo Szekely, Qiqiao Du, Xu Jing
{"title":"TRIB1 facilitates the proliferation and migration of ovarian cancer cells by inducing EMT progression.","authors":"Guangyan Shi, Kristian Holgersson, Zhen Xin, Laszlo Szekely, Qiqiao Du, Xu Jing","doi":"10.14670/HH-18-868","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>Ovarian cancer (OC) is a fatal female malignant tumor that severely impacts the health of women worldwide. Due to the lack of diagnostic biomarkers, 70% of OC patients are considered in the advanced stage at the first diagnosis. Exploring novel biomarkers for OC diagnosis has become an urgent clinical need to address. TRIB1 is a newly discovered oncogene in several malignant tumors, including acute myeloid leukemia, prostate cancer, and breast cancer. However, the biological function of TRIB1 in OC remains uncertain and, therefore, was explored in the present study.</p><p><strong>Methods: </strong>Levels of TRIB1 in OC and normal tissues were evaluated in the GEPIA database. TRIB1-KD was constructed in ES-2 cells and TRIB1-OE was constructed in OVCAR3 cells using a siRNA and OE vector, respectively. The proliferation ability was determined using the CCK-8 and clone formation assays. The migration ability was detected using the wound healing and Transwell assays. The expression of epithelial-mesenchymal transition (EMT) biomarkers was determined using western blotting.</p><p><strong>Results: </strong>TRIB1 was markedly upregulated in OC tissues compared with normal ovarian tissues in the GEPIA database. The TRIB1 level was slightly altered among ES-2, CAOV3, and SKOV3 cells, with the highest expression in ES-2 cells, which was greatly reduced in OVCAR3 cells. In TRIB1-KD ES-2 cells, a remarkably reduced proliferation ability was observed with the CCK-8 and clone formation assays, accompanied by a reduction in migration distance in the Wound healing assay and the number of migrated cells in the Transwell assay. In contrast, in TRIB1-OE OVCAR3 cells, increased proliferation ability was observed, accompanied by increased migration distance and number of migrated cells. Furthermore, EMT progression was markedly repressed in TRIB1-KD ES-2 cells and remarkably enhanced in TRIB1-OE OVCAR3 cells.</p><p><strong>Conclusion: </strong>TRIB1 facilitated the proliferation and migration of OC cells by enhancing EMT progression.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18868"},"PeriodicalIF":2.5000,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Histology and histopathology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.14670/HH-18-868","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Aim: Ovarian cancer (OC) is a fatal female malignant tumor that severely impacts the health of women worldwide. Due to the lack of diagnostic biomarkers, 70% of OC patients are considered in the advanced stage at the first diagnosis. Exploring novel biomarkers for OC diagnosis has become an urgent clinical need to address. TRIB1 is a newly discovered oncogene in several malignant tumors, including acute myeloid leukemia, prostate cancer, and breast cancer. However, the biological function of TRIB1 in OC remains uncertain and, therefore, was explored in the present study.

Methods: Levels of TRIB1 in OC and normal tissues were evaluated in the GEPIA database. TRIB1-KD was constructed in ES-2 cells and TRIB1-OE was constructed in OVCAR3 cells using a siRNA and OE vector, respectively. The proliferation ability was determined using the CCK-8 and clone formation assays. The migration ability was detected using the wound healing and Transwell assays. The expression of epithelial-mesenchymal transition (EMT) biomarkers was determined using western blotting.

Results: TRIB1 was markedly upregulated in OC tissues compared with normal ovarian tissues in the GEPIA database. The TRIB1 level was slightly altered among ES-2, CAOV3, and SKOV3 cells, with the highest expression in ES-2 cells, which was greatly reduced in OVCAR3 cells. In TRIB1-KD ES-2 cells, a remarkably reduced proliferation ability was observed with the CCK-8 and clone formation assays, accompanied by a reduction in migration distance in the Wound healing assay and the number of migrated cells in the Transwell assay. In contrast, in TRIB1-OE OVCAR3 cells, increased proliferation ability was observed, accompanied by increased migration distance and number of migrated cells. Furthermore, EMT progression was markedly repressed in TRIB1-KD ES-2 cells and remarkably enhanced in TRIB1-OE OVCAR3 cells.

Conclusion: TRIB1 facilitated the proliferation and migration of OC cells by enhancing EMT progression.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
TRIB1通过诱导EMT进展促进卵巢癌细胞的增殖和迁移。
目的:卵巢癌(OC)是一种严重影响全球女性健康的致死性恶性肿瘤。由于缺乏诊断性生物标志物,70%的OC患者在首次诊断时被认为处于晚期。探索用于卵巢癌诊断的新型生物标志物已成为迫切的临床需求。TRIB1是在急性髓性白血病、前列腺癌、乳腺癌等多种恶性肿瘤中新发现的致癌基因。然而,TRIB1在OC中的生物学功能仍不确定,因此本研究对其进行了探讨。方法:在GEPIA数据库中评估OC和正常组织中TRIB1的水平。用siRNA和OE载体分别在ES-2细胞和OVCAR3细胞中构建TRIB1-KD和TRIB1-OE。通过CCK-8和克隆形成实验确定其增殖能力。采用伤口愈合和Transwell试验检测迁移能力。western blotting检测上皮-间质转化(epithelial-mesenchymal transition, EMT)生物标志物的表达。结果:与GEPIA数据库中的正常卵巢组织相比,卵巢癌组织中的TRIB1明显上调。TRIB1在ES-2、CAOV3和SKOV3细胞中表达量略有变化,ES-2细胞中表达量最高,OVCAR3细胞中表达量大幅降低。在TRIB1-KD ES-2细胞中,CCK-8和克隆形成实验观察到增殖能力显著降低,伤口愈合实验中迁移距离减少,Transwell实验中迁移细胞数量减少。相比之下,TRIB1-OE OVCAR3细胞的增殖能力增强,迁移距离和迁移细胞数量增加。此外,在TRIB1-KD ES-2细胞中,EMT进展明显受到抑制,而在TRIB1-OE OVCAR3细胞中,EMT进展显著增强。结论:TRIB1通过促进EMT进展促进OC细胞的增殖和迁移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Histology and histopathology
Histology and histopathology 生物-病理学
CiteScore
3.90
自引率
0.00%
发文量
232
审稿时长
2 months
期刊介绍: HISTOLOGY AND HISTOPATHOLOGY is a peer-reviewed international journal, the purpose of which is to publish original and review articles in all fields of the microscopical morphology, cell biology and tissue engineering; high quality is the overall consideration. Its format is the standard international size of 21 x 27.7 cm. One volume is published every year (more than 1,300 pages, approximately 90 original works and 40 reviews). Each volume consists of 12 numbers published monthly online. The printed version of the journal includes 4 books every year; each of them compiles 3 numbers previously published online.
期刊最新文献
BPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1. Lymph node or lymphoid aggregate? Impact on cancer resection quality, clinical prognosis, and tumor staging. Advances in 3D bioprinting to enhance translational applications in bone tissue engineering and regenerative medicine. Prospects of induced pluripotent stem cells in treating advancing Alzheimer's disease: A review. Mechanism of PTPN18 for regulating the migration and invasion of endometrial cancer cells via the MYC/PI3K/AKT pathway.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1