BTBD7促进前列腺癌细胞上皮-间质转化、增殖和侵袭。

Q2 Medicine Journal of Buon Pub Date : 2021-09-01
Bin Chen, Chang Liu, Guohui Bai, Yuhang Zhu, Houqiang Xu
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引用次数: 0

摘要

目的:探讨BTBD7在前列腺癌(PCa)发生发展中的潜在功能及其分子机制。方法:采用qRT-PCR检测前列腺癌患者血清BTBD7水平。CCK-8法和Transwell法检测BTBD7对细胞活力和侵袭性的调控作用。此外,Western blot检测BTBD7干预PCa细胞上皮-间质转化(EMT)标志物E-cadherin和N-cadherin的蛋白水平。结果:前列腺癌患者血清BTBD7水平升高,尤其是Gleason评分≥8分或TNM分期Ⅲ+Ⅳ者。BTBD7的敲低降低了PCa细胞的活力和侵袭性,上调E-cadherin,下调N-cadherin。结论:前列腺癌患者血清BTBD7水平升高。它通过触发增生性和侵袭性潜能以及EMT来加速前列腺癌的发展。
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BTBD7 accelerates the epithelial-mesenchymal transition, proliferation and invasion of prostate cancer cells.

Purpose: To investigate the potential function of BTBD7 in prostate cancer (PCa) development and the underlying molecular mechanism.

Methods: Serum levels of BTBD7 in PCa patients were examined by qRT-PCR. Regulatory effects of BTBD7 on viability and invasiveness were detected by CCK-8 and Transwell assay, respectively. Moreover, Western blot analysis was conducted to examine protein levels of epithelial-mesenchymal transition (EMT) markers (E-cadherin and N-cadherin) in PCa cells intervened by BTBD7.

Results: Serum level of BTBD7 was increased in PCa patients, especially those with Gleason score ≥8 or TNM staging Ⅲ+Ⅳ. Knockdown of BTBD7 attenuated the viability and invasiveness of PCa cells, which upregulated E-cadherin and downregulated N-cadherin.

Conclusion: Serum level of BTBD7 increases in PCa patients. It accelerates PCa development by triggering proliferative and invasive potentials, as well as EMT.

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来源期刊
Journal of Buon
Journal of Buon 医学-肿瘤学
自引率
0.00%
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0
审稿时长
4-8 weeks
期刊介绍: JBUON aims at the rapid diffusion of scientific knowledge in Oncology. Its character is multidisciplinary, therefore all aspects of oncologic activities are welcome including clinical research (medical oncology, radiation oncology, surgical oncology, nursing oncology, psycho-oncology, supportive care), as well as clinically-oriented basic and laboratory research, cancer epidemiology and social and ethical aspects of cancer. Experts of all these disciplines are included in the Editorial Board. With a rapidly increasing body of new discoveries in clinical therapeutics, the molecular mechanisms that contribute to carcinogenesis, advancements in accurate and early diagnosis etc, JBUON offers a free forum for clinicians and basic researchers to make known promptly their achievements around the world. With this aim JBUON accepts a broad spectrum of articles such as editorials, original articles, reviews, special articles, short communications, commentaries, letters to the editor and correspondence among authors and readers. JBUON keeps the characteristics of its former paper print edition and appears as a bimonthly e-published journal with continuous volume, issue and page numbers.
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