The role of Circ_PRKCI/miR-24-3p in the metastasis of prostate cancer.

The role of Circ_PRKCI/miR-24-3p in the metastasis of prostate cancer.
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发表时间:
2021
期刊:
Journal of B.U.ON. : official journal of the Balkan Union of Oncology
影响因子:
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通讯作者:
M. Kong;Haijun Chen
M. Kong;Haijun Chen
中科院分区:
其他
文献类型:
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作者:
M. Kong;Haijun Chen

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目的探讨circ_PRKCI在前列腺癌(PCa)发生发展中的作用及其分子机制。方法检测40例PCa组织及癌旁正常组织中Circ_PRKCI的表达。探讨PCa患者circ-PRKCI水平与病理指标的关系。在DU-145和PC-3细胞中转染sh-circ_PRKCI后,检查活力、迁移和侵袭细胞的数量以及伤口闭合的变化。最后,circ_PRKCI的下游靶点通过双荧光素酶报告基因测定得到证实,并且它们参与PCa的发育最终通过拯救实验得到说明。结果Circ_PRKCI在PCa组织中的表达明显高于癌旁正常组织。高表达circ_PRKCI的PCa患者有较高的淋巴结转移和远处转移风险。circ_PRKCI基因的敲除可降低PCa细胞的增殖和转移能力。miR-24- 3 p作为circ_PRKCI的下游靶点,受其负调控,并且circ_PRKCI/miR-24- 3 p轴参与了PCa的增殖和转移潜能的触发。结论Circ_PRKCI在PCa组织中表达上调,其水平与PCa患者的转移率有关。它通过下调miR-24- 3 p触发PCa的增殖和转移潜能。
PURPOSE The purpose of this study was to explore the role of circ_PRKCI in regulating prostate cancer (PCa) development and the underlying molecular mechanism. METHODS Circ_PRKCI levels in 40 PCa tissues and adjacent normal ones were detected. The relationship between circ_PRKCI level and pathological indicators in PCa patients was explored. After transfection of sh-circ_PRKCI in DU-145 and PC-3 cells, changes in viability, numbers of migratory and invasive cells, and wound closure were examined. Finally, the downstream target of circ_PRKCI was confirmed by dual-luciferase reporter assay and their involvement in PCa development was finally illustrated by rescue experiments. RESULTS Circ_PRKCI was upregulated in PCa tissues than adjacent normal ones. PCa patients expressing a high level of circ_PRKCI had high risks of lymphatic metastasis and distant metastasis. Knockdown of circ_PRKCI weakened proliferative and metastatic abilities of PCa cells. As the downstream target of circ_PRKCI, miR-24-3p was negatively regulated by it. Moreover, circ_PRKCI/miR-24-3p axis was responsible for triggering proliferative and metastatic potentials in PCa. CONCLUSIONS Circ_PRKCI is upregulated in PCa tissues, and its level is linked to metastasis rate in PCa patients. It triggers proliferative and metastatic potentials in PCa by downregulating miR-24-3p.