miR-216b 通过靶向 PARK7 抑制胃癌的增殖和迁移。
MiR-216b inhibits gastric cancer proliferation and migration by targeting PARK7.
机构信息
Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, China.
出版信息
Indian J Pathol Microbiol. 2021 Jan-Mar;64(1):52-57. doi: 10.4103/IJPM.IJPM_777_19.
OBJECTIVE
Postoperative recurrence and metastasis of gastric cancer is still a difficult problem in medical field. About 60% of patients with advanced gastric cancer die from peritoneal metastasis, which has become one of the main causes of death of gastric cancer patients. To elucidate the molecular mechanism of peritoneal metastasis of gastric cancer can help us better early diagnosis and improve treatment measures.
METHODS
This project intends to validate the above hypothesis from three different levels of tissue, cell, and animal models by means of fluorescence quantitative PCR, Western blot, double Luciferase Report Analysis and immunohistochemical detection, and to further explore the molecular mechanism of peritoneal metastasis of gastric cancer.
RESULTS
Our previous studies have shown that PARK7 promotes peritoneal metastasis of gastric cancer through PI3K/Akt signaling pathway, but its specific regulatory mechanism remains unclear.
CONCLUSION
Our preliminary study showed that the expression of microRNA-216b in gastric cancer tissues with peritoneal metastasis was significantly lower than that in patients without peritoneal metastasis, while the expression of PARK7 was the opposite.
目的
胃癌术后复发和转移仍然是医学领域的难题。约 60%的晚期胃癌患者死于腹膜转移，这已成为胃癌患者死亡的主要原因之一。阐明胃癌腹膜转移的分子机制有助于我们更好地进行早期诊断和提高治疗措施。
方法
本项目拟通过荧光定量 PCR、Western blot、双荧光素酶报告分析和免疫组织化学检测等方法，从组织、细胞和动物模型三个不同水平验证上述假说，进一步探讨胃癌腹膜转移的分子机制。
结果
我们之前的研究表明，PARK7 通过 PI3K/Akt 信号通路促进胃癌腹膜转移，但具体的调控机制尚不清楚。
结论
我们的初步研究表明，具有腹膜转移的胃癌组织中 microRNA-216b 的表达明显低于无腹膜转移的患者，而 PARK7 的表达则相反。
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