共查询到20条相似文献,搜索用时 140 毫秒
1.
Long noncoding RNAs (lncRNAs) have been acknowledged as important regulators in various human cancers.
lncRNA MNX1-AS1 has been shown to be an oncogene in epithelial ovarian cancer. However, the function of MNX1-AS1 in glioblastoma (GBM) remains largely unknown. Here we found that the expression of
MNX1-AS1 was significantly upregulated in GBM tissues and cell lines. Knockdown of MNX1-AS1 significantly inhibited the proliferation, migration, and invasion of GBM cells. In terms of mechanism, we found that
MNX1-AS1 could bind to miR-4443 in GBM cells. Overexpression of miR-4443 significantly inhibited the
expression of MNX1-AS1 and vice versa. Moreover, there was an inverse correlation between the expression
levels of MNX1-AS1 and miR-4443 in GBM tissues. We found that overexpression of miR-4443 inhibited
the proliferation, migration, and invasion of GBM cells. We also showed that inhibition of miR-4443 reversed
the effects of MNX1-AS1 knockdown on GBM cell proliferation, migration, and invasion. Taken together, we
found that MNX1-AS1 promoted the proliferation, migration, and invasion of GBM cells through inhibiting
miR-4443. 相似文献
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miR-363-3p has been shown to suppress tumor growth and metastasis in various human cancers. However, the
function of miR-363-3p in osteosarcoma (OS) has not been determined. In our study, we found that the expression of miR-363-3p was significantly downregulated in OS tissues compared with adjacent normal tissues.
miR-363-3p expression was associated with the poor overall survival rate of OS patients. Moreover, we found
that overexpression of miR-363-3p markedly inhibited the proliferation, migration, and invasion of U2OS and
MG63 cells. Moreover, we found that SOX4 was a direct target of miR-363-3p in OS cells. Overexpression
of miR-363-3p significantly inhibited the expression of SOX4. Expression levels of miR-363-3p and SOX4
were negatively correlated in OS tissues. Finally, we found that restoration of SOX4 attenuated the suppressive
effects of miR-363-3p on the proliferation, migration, and invasion of U2OS and MG63 cells. Therefore, our
findings demonstrated that miR-363-3p served as a tumor suppressor in OS tissues by targeting SOX4. 相似文献
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miR-150 has been demonstrated to inhibit tumor progression in various human cancers, including colorectal
cancer, ovarian cancer, and thyroid cancer. However, the role of miR-150 in melanoma remains to be determined. In this study, we found that miR-150 was underexpressed in melanoma tissues and cell lines. Through
transfection of miR-150 mimics, we found that miR-150 significantly inhibited the proliferation, migration,
and invasion of melanoma cells. In mechanism, we found that MYB was a target of miR-150 in melanoma
cells. Overexpression of miR-150 significantly inhibited mRNA and protein levels of MYB in melanoma cells.
Moreover, there was an inverse correlation between the expression of miR-150 and MYB in melanoma tissues.
We also showed that MYB was upregulated in melanoma tissues and cell lines. Through functional experiments, we found that restoration of MYB in miR-150-overexpressed melanoma cells rescued the proliferation, migration, and invasion. Therefore, our findings demonstrated that miR-150 suppressed the proliferation,
migration, and invasion of melanoma cell by downregulating MYB. 相似文献
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Previous studies have reported that miR-615 exerts a tumor suppressor role in some tumors, such as esophageal
squamous cell carcinoma and non-small cell lung cancer. However, the role of miR-615 in prostate cancer has
not been defined. Here we found that miR-615 was downregulated in prostate cancer tissues and cell lines.
Overexpression of miR-615 in PC-3 cells significantly inhibited cellular proliferation, migration, and invasion.
Moreover, overexpression of miR-615 delayed tumor growth in vivo. In terms of mechanism, we found that
cyclin D2 (CCND2) is a target gene of miR-615 in prostate cancer. We showed that miR-615 could bind to
the 3 -UTR region of CCND2 mRNA and inhibit its expression. There was a negative correlation between the
expression of miR-615 and CCND2 in prostate cancer tissues. Moreover, restoration of cyclin D2 abolished
the inhibitory effects of miR-615 on the proliferation, migration, and invasion of prostate cancer cells. Taken
together, our study identified miR-615 as a tumor suppressor by targeting cyclin D2 in prostate cancer. 相似文献
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Jingyuan Li Lijuan Wang Zongzhi Liu Chao Zu Fanfan Xing Pei Yang Yongkang Yang Xiaoqian Dang Kunzheng Wang 《Oncotarget》2015,6(28):26216-26229
Accumulating evidence indicates that dysregulation of miRNAs could contribute to tumor growth and metastasis of chondrosarcoma by infuencing cell proliferation and invasion. In the current study, we are interested to examine the role of miRNAs in the carcinogenesis and progression of chondrosarcoma. Here, using comparative miRNA profiling of tissues and cells of chondrosarcoma and cartilage, we identified miR-494 as a commonly downregulated miRNA in the tissues of patients with chondrosarcoma and chondrosarcoma cancer cell line, and upregulation of miR-494 could inhibit proliferation and invasion of chondrosarcoma cancer cells in vivo and in vitro. Moreover, our data demonstrated that SOX9, the essential regulator of the process of cartilage differentiation, was the direct target and functional mediator of miR-494 in chondrosarcoma cells. And downregulation of SOX9 could also inhibit migration and invasion of chondrosarcoma cells. In the last, we identified low expression of miR-494 was significantly correlated with poor overall survival and prognosis of chondrosarcoma patients. Thus, miR-494 may be a new common therapeutic target and prognosis biomarker for chondrosarcoma. 相似文献
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Fadila Guessous Melissa Alvarado-Velez Lukasz Marcinkiewicz Ying Zhang Jungeun Kim Simon Heister Benjamin Kefas Jakub Godlewski David Schiff Benjamin Purow Roger Abounader 《Journal of neuro-oncology》2013,112(2):153-163
MicroRNAs and cancer stem cells have emerged as critical players in glioblastoma, one of the deadliest human cancers. In this study, we investigated the expression and function of microRNA-10b in glioblastoma cells and stem cells. An analysis of The Cancer Genome Atlas data revealed a correlation between high miR-10b levels and poor prognosis in glioblastoma patients. We measured the levels of miR-10b and found that it is upregulated in human glioblastoma tissues, glioblastoma cell and stem cell lines as compared to normal human tissues or astrocytes. Inhibition of miR-10b with a specific antagomir inhibited the proliferation of glioblastoma established and stem cell lines. Inhibition of miR-10b strongly reduced cell invasion and migration in glioblastoma cell and stem cell lines while overexpression of miR-10b induced cell migration and invasion. We also investigated several predicted targets of miR-10b but could not verify any of them experimentally. Additionally, miR-10b inhibition significantly decreased the in vivo growth of stem cell-derived orthotopic GBM xenografts. Altogether, our findings confirm the oncogenic effects of miR-10b in GBM cells and show for the first time a role of this microRNA in GBM stem cells. Targeting miR-10b might therefore inhibit glioblastoma stem cells, which are thought to be at the origin of glioblastoma and to contribute its recurrence and resistance to therapy. 相似文献
11.
目的:探讨miRNA通过靶向调控促癌基因SOX9的表达影响胶质瘤生物学行为的作用及机制。方法:采用qRT-PCR检测miR-223在WHO分级低级别(Ⅰ和Ⅱ)与高级别(Ⅲ和Ⅳ)脑胶质瘤组织和癌旁正常组织中的表达水平,miR-223在正常人星形胶质细胞、A172、U251、U87和U373胶质瘤细胞中的表达水平。采用生物信息软件预测SOX9是miR-223的潜在靶基因,并通过双荧光素酶报告基因实验进行验证。采用qRT-PCR、Western blot检测SOX9在各WHO分级脑胶质瘤组织和各脑胶质瘤细胞株中的表达。多种体外实验检测miR-223和SOX9对脑胶质瘤细胞增殖,侵袭、迁移及周期的影响。构建脑胶质瘤裸鼠移植瘤模型,检测miR-223对体内移植瘤生长的影响。结果:miR-223在脑胶质瘤组织及脑胶质瘤细胞中均呈现低表达,并且通过抑制靶基因SOX9的靶向调控作用抑制脑胶质瘤细胞恶性生物学行为。同时脑胶质瘤裸鼠移植瘤模型中,miR-223过表达可下调SOX9的表达水平并抑制裸鼠体内移植瘤的生长。结论:miR-223通过抑制靶基因SOX9的表达水平在胶质瘤中扮演抑癌基因的角色,提示其具有成为胶质瘤诊疗新靶点的潜力。 相似文献
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MicroRNA-132 (miR-132) has been demonstrated to be a tumor suppressor in several types of tumors. However,
the expression and the role of miR-132 in human thyroid cancer are still poorly understood. The aim of the
present study was to examine the potential roles and molecular mechanism of miR-132 in thyroid cancer. We
found that miR-132 expression levels were significantly downregulated in thyroid cancer tissues and cell lines.
Function assays showed that overexpression of miR-132 in TPC1 cells inhibited cell proliferation, migration,
and invasion. Forkhead box protein A1 (FOXA1) was identified as a direct target of miR-132 in thyroid cancer
cells. Knockdown of FOXA1 in TPC1 cells significantly inhibited cell proliferation, migration, and invasion,
which mimicked the suppressive effect induced by miR-132 overexpression. Restoration of FOXA1 expression
partially reversed the suppressive effect induced by miR-132 overexpression. Taken together, these results suggested that miR-132 acts as a tumor suppressor in thyroid cancer through targeting FOXA1. 相似文献
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MicroRNA-132 (miR-132) has been demonstrated to be a tumor suppressor in several types of tumors. However,
the expression and the role of miR-132 in human thyroid cancer are still poorly understood. The aim of the
present study was to examine the potential roles and molecular mechanism of miR-132 in thyroid cancer. We
found that miR-132 expression levels were significantly downregulated in thyroid cancer tissues and cell lines.
Function assays showed that overexpression of miR-132 in TPC1 cells inhibited cell proliferation, migration,
and invasion. Forkhead box protein A1 (FOXA1) was identified as a direct target of miR-132 in thyroid cancer
cells. Knockdown of FOXA1 in TPC1 cells significantly inhibited cell proliferation, migration, and invasion,
which mimicked the suppressive effect induced by miR-132 overexpression. Restoration of FOXA1 expression
partially reversed the suppressive effect induced by miR-132 overexpression. Taken together, these results suggested that miR-132 acts as a tumor suppressor in thyroid cancer through targeting FOXA1. 相似文献
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Yue Zhang Fu-Jun Zhao Li-Lan Chen Luo-Qiao Wang Kenneth P. Nephew Ying-Li Wu Shu Zhang 《Oncotarget》2014,5(23):12291-12303
Metastasis is major cause of mortality in patients with ovarian cancer. MiR-373 has been shown to play pivotal roles in tumorigenesis and metastasis; however, a role for miR-373 in ovarian cancer has not been investigated. In this study, we show that the miR-373 expression is down-regulated in human epithelial ovarian cancer (EOC) and inversely correlated with clinical stage and histological grade. Ectopic overexpression of miR-373 in human EOC cells suppressed cell invasion in vitro and metastasis in vivo, and the epithelial–mesenchymal transition process. Silencing the expression of miR-373 resulted in an increased migration and invasion of EOC cells. Using integrated bioinformatics analysis, gene expression arrays, and luciferase assay, we identified Rab22a as a direct and functional target of miR-373 in EOC cells. Expression levels of miR-373 were inversely correlated with Rab22a protein levels in human EOC tissues. Rab22a knockdown inhibited invasion and migration of EOC cells, increased E-cadherin expression, and suppressed the expression of N-cadherin. Moreover, overexpression of Rab22a abrogated miR-373-induced invasion and migration of EOC cells. Taken together, these results demonstrate that miR-373 suppresses EOC invasion and metastasis by directly targeting Rab22a gene, a new potential therapeutic target in EOC. 相似文献
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目的:探讨lncRNA 母源性印记基因3(maternal imprinting gene 3, MEG3)通过miR-9-5p/SOCS5 轴对宫颈癌细胞增殖、迁移、侵袭和上皮间质转化(epithelial-mesenchymal transition, EMT)的调控作用。方法: 收集2017 年1 月至2019 年6 月重庆市中医院手术切除的20 例宫颈癌患者的癌及癌旁组织标本;利用脂质体转染技术分别将pcDNA3.1-MEG3、si-MEG3、miR-9-5p mimics、miR-9-5p inhibitor 及其对照质粒等转染进宫颈癌HeLa 和SiHa 细胞,构建过表达和沉默细胞模型。用qPCR检测宫颈癌组织及细胞模型中MEG3、miR-9-5p 和SOCS5 表达水平,用CCK-8 法、Transwell 小室法检测细胞的增殖、迁移和侵袭能力,用细胞免疫荧光实验检测细胞中E-cadherin 和vimentin 表达水平。通过在线生物信息学TargetScan 数据库预测靶基因,用双荧光素酶报告基因实验验证miR-9-5p 分别与MEG3 和SOCS5 的靶向关系。结果: 分别与癌旁组织和宫颈上皮HcerEpic 细胞比较,宫颈癌组织和细胞系中MEG3 和SOCS5 表达显著下调、miR-9-5p 表达显著上调(均P<0.01)。TargetScan 数据库分析和双荧光素酶报告基因实验证实miR-9-5p 与MEG3 或SOCS5 存在靶向关系。MEG3 和SOCS5 显著抑制宫颈癌细胞的增殖、迁移与侵袭能力(均P<0.01),miR-9-5p 显著提高细胞的增殖、迁移与侵袭能力(均P<0.01)。MEG3 和SOCS5 促进E-cadherin 表达、抑制vimentin表达;miR-9-5p 抑制E-cadherin 表达、促进vimentin 表达(P<0.05 或P<0.01)。结论: lncRNA MEG3 通过miR-9-5p/SOCS5 分子轴调控宫颈癌细胞的增殖、迁移、侵袭与EMT进程。 相似文献
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Yue-chao Fan Peng-jin Mei Chen Chen Fa-an Miao Hui Zhang Zhong-lin Li 《Journal of neuro-oncology》2013,115(2):179-188
Previous studies reported that miR-29c is significantly downregulated in several tumors. However, little is known about the effect and molecular mechanisms of action of miR-29c in human glioma. Using quantitative RT-PCR, we demonstrated that miR-29c was significantly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues (P < 0.05, χ2 test). Overexpression of miR-29c dramatically reduced the proliferation and caused cessation of cell cycle. The reduced cell proliferation is due to G1 phase arrest as cyclin D1 and cyclin E are diminished whereas p27 and p21 are upregulated. We further demonstrated that miR-29c overexpression suppressed the glioma cell migration and invasion abilities by targeting MMP-2. In addition, we also found that overexpression of miR-29c sharply inhibited angiogenesis, which correlated with down-regulation of VEGF. The data indicate that miR-29c may be a tumor suppressor involved in the progression of glioma. 相似文献