Maolan Zeng, Yanhua Zhou, Yinxia Zhang, Tiancheng Wang, Jing Wang
{"title":"miR-489 在胰腺癌增殖和凋亡中的作用","authors":"Maolan Zeng, Yanhua Zhou, Yinxia Zhang, Tiancheng Wang, Jing Wang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>The purpose of the present study was to detect the expression of miR-489 in pancreatic cancer (PC) tissues and cells, and to explore the effects of miR-489 on cell proliferation and apoptosis of human PC cells and to also uncover the underlying mechanism.</p><p><strong>Methods: </strong>miR-489 expression was assessed by quantitative real time-polymerase chain reaction (qRT-PCR) in PC tissues and PANC-1 and HPDE6-C7 cell lines. The binding-site predictions by bioinformatics showed that AKT Serine/Threonine Kinase 3 (AKT3) might be a potential target of miR-489. AKT3 expression in PC tissues and cells was detected by qRT-PCR, luciferase report assay and Western blotting assay were used to verify the rationality of the target gene. The biological role of miR-489 on cell proliferation, cell cycle and apoptosis were determined in PANC-1 cells by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry after transfection with miR-NC, miR-489 mimics and si-AKT3.</p><p><strong>Results: </strong>Compared with normal adjacent tissues and normal pancreatic cells, the expression of miR-489 was markedly down-regulated in PC tissues and cells. AKT3 was considered as a downstream gene of miR-489 and it was found that the expression levels of miR-489 and AKT3 were inversely proportional to each other, which was further confirmed by luciferase and Western blot assays. In subsequent experiments, up-regulation of miR-489 by transfection with miR-489 mimics significantly inhibited cell proliferation, blocked the G1/S transition and induced cell apoptosis of PANC-1 cells. However, overexpression of AKT3 significantly counteracted the biological effects of miR-489.</p><p><strong>Conclusions: </strong>Our findings indicate that up-regulation of miR-489 could suppress PC cell proliferation and facilitate cell apoptosis through targeting AKT3. miR-489 and AKT3 might serve as potential targets in the therapy of PC.</p>","PeriodicalId":94065,"journal":{"name":"Journal of B.U.ON. : official journal of the Balkan Union of Oncology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2019-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Role of miR-489 in the proliferation and apoptosis of pancreatic carcinoma.\",\"authors\":\"Maolan Zeng, Yanhua Zhou, Yinxia Zhang, Tiancheng Wang, Jing Wang\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>The purpose of the present study was to detect the expression of miR-489 in pancreatic cancer (PC) tissues and cells, and to explore the effects of miR-489 on cell proliferation and apoptosis of human PC cells and to also uncover the underlying mechanism.</p><p><strong>Methods: </strong>miR-489 expression was assessed by quantitative real time-polymerase chain reaction (qRT-PCR) in PC tissues and PANC-1 and HPDE6-C7 cell lines. The binding-site predictions by bioinformatics showed that AKT Serine/Threonine Kinase 3 (AKT3) might be a potential target of miR-489. AKT3 expression in PC tissues and cells was detected by qRT-PCR, luciferase report assay and Western blotting assay were used to verify the rationality of the target gene. The biological role of miR-489 on cell proliferation, cell cycle and apoptosis were determined in PANC-1 cells by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry after transfection with miR-NC, miR-489 mimics and si-AKT3.</p><p><strong>Results: </strong>Compared with normal adjacent tissues and normal pancreatic cells, the expression of miR-489 was markedly down-regulated in PC tissues and cells. AKT3 was considered as a downstream gene of miR-489 and it was found that the expression levels of miR-489 and AKT3 were inversely proportional to each other, which was further confirmed by luciferase and Western blot assays. In subsequent experiments, up-regulation of miR-489 by transfection with miR-489 mimics significantly inhibited cell proliferation, blocked the G1/S transition and induced cell apoptosis of PANC-1 cells. However, overexpression of AKT3 significantly counteracted the biological effects of miR-489.</p><p><strong>Conclusions: </strong>Our findings indicate that up-regulation of miR-489 could suppress PC cell proliferation and facilitate cell apoptosis through targeting AKT3. miR-489 and AKT3 might serve as potential targets in the therapy of PC.</p>\",\"PeriodicalId\":94065,\"journal\":{\"name\":\"Journal of B.U.ON. : official journal of the Balkan Union of Oncology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of B.U.ON. : official journal of the Balkan Union of Oncology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of B.U.ON. : official journal of the Balkan Union of Oncology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Role of miR-489 in the proliferation and apoptosis of pancreatic carcinoma.
Purpose: The purpose of the present study was to detect the expression of miR-489 in pancreatic cancer (PC) tissues and cells, and to explore the effects of miR-489 on cell proliferation and apoptosis of human PC cells and to also uncover the underlying mechanism.
Methods: miR-489 expression was assessed by quantitative real time-polymerase chain reaction (qRT-PCR) in PC tissues and PANC-1 and HPDE6-C7 cell lines. The binding-site predictions by bioinformatics showed that AKT Serine/Threonine Kinase 3 (AKT3) might be a potential target of miR-489. AKT3 expression in PC tissues and cells was detected by qRT-PCR, luciferase report assay and Western blotting assay were used to verify the rationality of the target gene. The biological role of miR-489 on cell proliferation, cell cycle and apoptosis were determined in PANC-1 cells by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay and flow cytometry after transfection with miR-NC, miR-489 mimics and si-AKT3.
Results: Compared with normal adjacent tissues and normal pancreatic cells, the expression of miR-489 was markedly down-regulated in PC tissues and cells. AKT3 was considered as a downstream gene of miR-489 and it was found that the expression levels of miR-489 and AKT3 were inversely proportional to each other, which was further confirmed by luciferase and Western blot assays. In subsequent experiments, up-regulation of miR-489 by transfection with miR-489 mimics significantly inhibited cell proliferation, blocked the G1/S transition and induced cell apoptosis of PANC-1 cells. However, overexpression of AKT3 significantly counteracted the biological effects of miR-489.
Conclusions: Our findings indicate that up-regulation of miR-489 could suppress PC cell proliferation and facilitate cell apoptosis through targeting AKT3. miR-489 and AKT3 might serve as potential targets in the therapy of PC.