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miR-497-5p 通过靶向 PDK3 抑制胃癌细胞的增殖和生长。

miR-497-5p inhibits gastric cancer cell proliferation and growth through targeting PDK3.

机构信息

Department of Infection Medicine, First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang Province, People's Republic of China.

Department of Immunology, Basic Medical College, Jiamusi University, Jiamusi, Heilongjiang Province, People's Republic of China

出版信息

Biosci Rep. 2019 Sep 6;39(9). doi: 10.1042/BSR20190654. Print 2019 Sep 30.

DOI:10.1042/BSR20190654
PMID:31409724
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6732365/
Abstract

MicroRNA plays an important role in gastric cancer (GC) development, while the function of miR-497-5p in this disease remains unknown. In the present study, we demonstrated miR-497-5p as a tumor suppressive microRNA in GC. miR-497-5p was down-regulated in GC tissues and its expression was associated with the disease stage. Inhibition of miR-497-5p promoted GC cell proliferation and growth. By contrast, miR-497-5p ectopic expression suppressed the proliferation and growth of GC cells. In addition, miR-497-5p inhibited DNA synthesis and enhanced apoptosis in GC cells. The cell cycle progression was suppressed by miR-497-5p. Mechanistically, miR-497-5p directly targeted and suppressed the expression of pyruvate dehydrogenase kinase 3 (PDK3), which is highly expressed in GC tissues. Over-expression of PDK3 promoted the proliferation of GC cells. Our study revealed that miR-497-5p inhibited GC cell proliferation and growth via targeting PDK3.

摘要

微小 RNA 在胃癌 (GC) 发展中发挥重要作用,而 miR-497-5p 在该疾病中的功能尚不清楚。在本研究中,我们证明 miR-497-5p 是 GC 中的一种肿瘤抑制 microRNA。miR-497-5p 在 GC 组织中下调,其表达与疾病分期相关。抑制 miR-497-5p 促进 GC 细胞增殖和生长。相比之下,miR-497-5p 的异位表达抑制了 GC 细胞的增殖和生长。此外,miR-497-5p 抑制了 GC 细胞的 DNA 合成并增强了其凋亡。miR-497-5p 抑制了细胞周期进程。在机制上,miR-497-5p 可直接靶向并抑制丙酮酸脱氢酶激酶 3 (PDK3) 的表达,该基因在 GC 组织中高度表达。PDK3 的过表达促进了 GC 细胞的增殖。我们的研究表明,miR-497-5p 通过靶向 PDK3 抑制 GC 细胞的增殖和生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/b8354157afdb/bsr-39-bsr20190654-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/a473223c91d8/bsr-39-bsr20190654-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/3c0cc8737b02/bsr-39-bsr20190654-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/bcc1d9d1534c/bsr-39-bsr20190654-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/ea7389d07052/bsr-39-bsr20190654-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/a680a95888f6/bsr-39-bsr20190654-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/b8354157afdb/bsr-39-bsr20190654-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/a473223c91d8/bsr-39-bsr20190654-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/3c0cc8737b02/bsr-39-bsr20190654-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/bcc1d9d1534c/bsr-39-bsr20190654-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/ea7389d07052/bsr-39-bsr20190654-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/a680a95888f6/bsr-39-bsr20190654-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a75d/6732365/b8354157afdb/bsr-39-bsr20190654-g6.jpg

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