MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

Chen, Haiwen; Luo, Qidong; Li, Hongliang

doi:10.1177/1010428317695941

Cited by 11 publications

(8 citation statements)

References 27 publications

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“…Both miR590-5p and miR-590-3p were found to participate in the carcinogenesis of different cancers, such as prostate cancer, liver cancer, lung cancer, etc. (Wang et al, 2016;Chen et al, 2017;Ge and Gong, 2017). A most recent study found miR590-5p inhibited colorectal cancer angiogenesis through the NF90/VEGFA signal (Zhou et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA LINC00657 Acting as a miR-590-3p Sponge to Facilitate Low Concentration Oxidized Low-Density Lipoprotein–Induced Angiogenesis

Bao

Huang

et al. 2018

Mol Pharmacol

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Angiogenesis in atherosclerotic plaque promotes plaque growth, causes plaque hemorrhage, and violates plaque stability. LINC00657 is a long noncoding RNA highly conserved and abundantly expressed in vascular endothelial cells. The present study was designed to investigate the effects and mechanisms of LINC00675 on low concentrations of oxidized low-density lipoprotein (oxLDL)-induced angiogenesis. Cell proliferation, transwell, wound healing, and tube formation assays were conducted to detect the effects of low concentrations of oxLDL on angiogenesis; the results discovered that oxLDL promoted cell proliferation, migration, and tube formation. oxLDL also upregulated LINC00657 expression. Inhibition of LINC00657 by siRNA significantly suppressed oxLDL-induced endothelial cell proliferation, migration, and tube formation. Bioinformatic assay indicated six binding sites in the LINC00657 sequence to miR-590-3p. The upregulation of LINC00657 was related to the downregulation of miR-590-3p in oxLDL-treated endothelial cells; while downregulation of LINC00657 resulted in upregulation of miR-590-3p. The antiangiogenesis effects of si-LINC00657 were partly abrogated by miR-590-3p inhibitor. Further dual-luciferase assay found miR-590-3p inhibited the expression of hypoxia-inducible factor 1 (HIF-1) by binding to the position of 689-696 in HIF-1 3'-untranslated region directly. MiR-590-3p also inhibited the oxLDL-induced upregulation of HIF-1, vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2), and matrix metalloproteinase-9 (MMP-9). These results suggested that in oxLDL-treated endothelial cells, LINC00657 acted as a miR-590-3p sponge to attenuate the suppression of miR-590-3p on HIF-1, and to promote angiogenesis through VEGF, MMP-2, and MMP-9. The present study provided new insight into the roles of LINC00657 and miR-590-3p in preventing oxLDL-induced angiogenesis and may provide a novel strategy for atherosclerosis treatment.

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Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA LINC00657 Acting as a miR-590-3p Sponge to Facilitate Low Concentration Oxidized Low-Density Lipoprotein–Induced Angiogenesis

Bao

Huang

et al. 2018

Mol Pharmacol

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“…Studies demonstrated that miR-590-3p was dysregulated in development of some cancers and suppressed evolution and progression of hepatocellular carcinoma [ 14 ], bladder cancer [ 18 ] and glioblastoma [ 19 ], meanwhile, might play an oncogene role in prostate cancer [ 15 ]. Consequently, the detailed role of miR-590-3p in malignancies still remains controversial.…”

Section: Discussionmentioning

confidence: 99%

“…In terms of mechanism, overexpression of miRNA-590-3p might promote the growth of tumor cells by targeting TFAM in colon cancer [ 21 ]. Chen et al pointed out that miR-590-3p up-regulation promoted cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells [ 15 ]. Pang et al demonstrated that miR-590-3p suppressed cancer cell migration, invasion and epithelial-mesenchymal transition in glioblastoma multiforme by inhibiting ZEB1 and ZEB2 [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

“…Ge et al found that over-expressed miR-590-3p enhanced the antitumor activity in the human tumor of hepatocellular carcinoma [ 14 ], and then upregulated cell migration, invasion and proliferation. However, Chen et al said that miR-590-3p might play the anti-oncogene role in prostate cancer and further repress the tumorgenesis and mobility [ 15 ]. Herein, whether miR-590-3p is a contributing factor of CRC evolution and progression or not remains controversial.…”

Section: Introductionmentioning

confidence: 99%

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MiR-590-3p promotes proliferation and metastasis of colorectal cancer via Hippo pathway

et al. 2017

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Studies reported that miR-590-3p was involved in human cancer progression. However, its roles of oncogene or anti-oncogene in malignancies still remain elusive. This study was aimed to investigate the effect of miR-590-3p on the cell proliferation and metastasis via Hippo pathway in colorectal cancer (CRC). In our study, miR-590-3p was demonstrated highly expressed in CRC tissues, compared with adjacent normal tissues (P<0.05). In addition, miR-590-3p was positively associated with TNM stage and distant metastasis. Survival analysis showed that high miR-590-3p was related with poor overall survival rate. Then, over-expressed miR-590-3p was demonstrated to promote proliferation, invasion and migration of colon caner cells. What’s more, MST1, LATS1 and SAV1 mRNA were showed lowly expressed and YAP1 expression in mRNA and protein levels were highly expressed in CRC tissues, compared with adjacent normal tissues (all P<0.05). miR-590-3p expression was negatively associated with LATS1 and SAV1 mRNA respectively and positively related with YAP1 mRNA in CRC tissues, meanwhile, there was no relationship between miR-590-3p and MST1 mRNA. Furthermore, over-expressing miR-590-3p inhibited expressions of LATS1 and SAV1, promoted YAP1 expression and didn’t effect MST1 expression in colon cancer cells. And luciferase assay showed that miR-590-3p over-expression inhibited the luciferase activity of LATS1 and SAV1 3’UTR, meanwhile it had no effect on the mutated form of these two plasmids. Taken together, these data suggest that highly-expressed miR-590-3p promotes biological effect of proliferation and metastasis via targeting Hippo pathway, and predicts worse clinical outcomes of CRC patients.

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“…For instance, miR-494 suppressed the proliferation and induced apoptosis of ovarian cancer cells, through negatively regulating the fibroblast growth factor receptor 2 oncogene (18). By contrast, several highly expressed miRNAs function as oncogenes during tumor development by repressing tumor suppressor genes (19)(20)(21). For instance, miR-130a enhances the proliferation and migration of gastric cancer cells by targeting transforming growth factor β receptor (TGFβR) 2 (22).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-219 is downregulated in non-small cell lung cancer and inhibits cell growth and metastasis by targeting HMGA2

Sun

Liu

et al. 2017

Molecular Medicine Reports

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Lung cancer is the most commonly diagnosed cancer and the leading cause of cancer-associated mortality worldwide. Non-small cell lung cancer (NSCLC) is the predominant type of lung cancer, and accounts for ~85% of all lung cancer cases. An increasing number of studies suggest that microRNAs (miRs) may be involved in the regulation of NSCLC carcinogenesis and progression. However, the expression and function of miRNA-219 in NSCLC, and its underlying mechanisms of action, remain unknown. In the present study, miR-219 expression in NSCLC tissues and cell lines was determined using reverse transcription-quantitative polymerase chain reaction. Following transfection with miR-219 mimics, the effects of miR-219 overexpression on NSCLC cell proliferation, migration and invasion were examined. Furthermore, the miR-219 target in NSCLC was investigated. miR-219 was observed to be downregulated in NSCLC tissues and NSCLC cell lines. In addition, miR-219 was demonstrated to function as a tumor suppressor in NSCLC, through inhibiting cell proliferation, migration and invasion in vitro. Furthermore, high mobility group AT-hook 2 (HMGA2) was identified to be a direct target of miR-219 in NSCLC, and downregulation of HMGA2 suppressed NSCLC cell proliferation, migration and invasion in vitro. HMGA2 expression was upregulated in NSCLC tissues, and was inversely correlated with miR-219 expression. In conclusion, miR-219 functions as a tumor suppressor and may be important in inhibiting the growth and metastasis of NSCLC cells via directly targeting HMGA2. Therefore, miR-219 may present a potential novel therapeutic target for NSCLC.

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MicroRNA-590-3p promotes cell proliferation and invasion by targeting inositol polyphosphate 4-phosphatase type II in human prostate cancer cells

Cited by 11 publications

References 27 publications

Long Noncoding RNA LINC00657 Acting as a miR-590-3p Sponge to Facilitate Low Concentration Oxidized Low-Density Lipoprotein–Induced Angiogenesis

Long Noncoding RNA LINC00657 Acting as a miR-590-3p Sponge to Facilitate Low Concentration Oxidized Low-Density Lipoprotein–Induced Angiogenesis

MiR-590-3p promotes proliferation and metastasis of colorectal cancer via Hippo pathway

MicroRNA-219 is downregulated in non-small cell lung cancer and inhibits cell growth and metastasis by targeting HMGA2

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