miR-217 targeting Wnt5a in osteosarcoma functions as a potential tumor suppressor

Wei, Renxiong; Deng, Zhouming; Su, Jiajia

doi:10.1016/j.biopha.2015.04.012

Cited by 32 publications

(19 citation statements)

References 21 publications

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“…Interestingly, miR-217 is down-regulated by cigarette smoke [40]. miR-217 was suggested to be a tumor suppressor by targeting Wnt5a in osteosarcoma and targeting IGF1R in ovarian cancer [41, 42]. …”

Section: Discussionmentioning

confidence: 99%

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

et al. 2017

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Triple negative breast cancer (TNBC) is one of the most aggressive breast cancers without effective targeted therapies. Numerous studies have implied that KLF5 plays an important roles in TNBC. How is KLF5 regulated by microRNAs has not been well studied. Here, we demonstrated that miR-217 down-regulates the expression of KLF5 and KLF5’s downstream target gene FGF-BP and Cyclin D1 in TNBC cell lines HCC1806 and HCC1937. Consequently, miR-217 suppresses TNBC cell growth, migration, and invasion. MiR-217 suppresses TNBC, at least partially, through down-regulating the KLF5 expression. These results suggest that the miR-217-KLF5 axis might serve as a potential target for treatment of TNBC.

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Section: Discussionmentioning

confidence: 99%

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

et al. 2017

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“…MiRNAs play a crucial role in cancer development process such as differentiation, proliferation and metastasis . According to previous studies, microRNA 217 (miR‐217) was linked with cell progression as a tumour suppressor . But, the mechanism of miR‐217 is still not clear in HCC.…”

Section: Introductionmentioning

confidence: 99%

“…12 According to previous studies, microRNA 217 (miR-217) was linked with cell progression as a tumour suppressor. 13,14 But, the mechanism of miR-217 is still not clear in HCC.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR‐217/MAPK1 axis

Wang

Guo

et al. 2018

J Cellular Molecular Medi

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Hepatocellular carcinoma (HCC) is an invasive malignant tumour and the second major cause of cancer‐related deaths over the world. CRNDE and miR‐217 are non‐coding RNAs which play critical roles in cell growth, proliferation, migration. Mitogen‐activated protein kinase 1 (MAPK1) also participates in cancer cell process. Hence, this study aimed at investigating the effect of CRNDE on migration and invasion of HCC and figuring out the role of miR‐217 and MAPK1 in this process. The overexpression of CRNDE was demonstrated by a microarray‐based lncRNA profiling study. CRNDE expression in HCC was verified by qRT‐PCR. MTT assay and BrdU staining were applied to detect cell proliferation level. Transwell assay was utilized to examine cell migration and invasiveness abilities. Wound healing assay was performed for further exploration of cell migration capacity. MiR‐217 was predicted by bioinformatics. The dual luciferase reporter assay was performed to corroborate the targeting relationship between CRNDE, miR‐217 and MAPK1. MAPK1, the downstream target of miR‐217, was predicted using bioinformatics and was further confirmed by qRT‐PCR and Western blot. The interaction between CRNDE, miR‐217 and MAPK1 was studied by qRT‐PCR, Western blot, MTT, BrdU, transwell assay and wound healing assay. CRNDE was up‐regulated in HCC tissues and HCC cell lines. The high expression of CRNDE facilitated cell proliferation, migration and invasion, while the inhibited one affected on the contrary. MiR‐217, negatively correlated with CRNDE expression, was the target of CRNDE and was more lowly expressed in HCC. With the high expression of miR‐217, HCC cell proliferation, migration and invasion were suppressed. MAPK1, the possible target of miR‐217, was negatively correlated with miR‐217 but positively correlated with CRNDE and had the same effect in HCC formation process as CRNDE. Long non‐coding RNA CRNDE promotes the proliferation, migration and invasion of HCC cells through miR‐217/MAPK1 axis.

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“…For example, in human osteosarcoma, the expression level of miR-217 was decreased in tumor tissues and cell lines. Decreased miR-217 expression was closely correlated with large tumor size, positive distant metastasis, advanced clinical stage and shorter overall survival (21,22). These findings suggest that in osteosarcoma, miR-217 may be involved in the initiation and progression of cancer, and could be investigated as a prognostic biomarker in the future (23).…”

Section: Discussionmentioning

confidence: 79%

“…In addition, in gastric cancer, upregulation of miR-217 significantly suppressed cell growth and invasion through negative regulation of . miR-217 has been verified as a tumor suppressor in osteosarcoma via blockade of the WAS protein family member 3 and Wnt5a (21,22,30). In colorectal cancer, enforced miR-217 expression targeted astrocyte-elevated gene-1 to decrease cell growth, colony formation, migration and invasion by promoting apoptosis and G 0 /G 1 phase arrest (24).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA 217 inhibits cell proliferation and enhances chemosensitivity to doxorubicin in acute myeloid leukemia by targeting KRAS

Xiao

Deng

et al. 2017

Oncology Letters

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Abstract. Acute myeloid leukemia (AML) is a heterogeneous malignant disorder derived from the myeloid hematopoietic cells that accounts for ~80% of all adult acute leukemia. Numerous studies have shown that drug resistance not only exists against conventional chemotherapeutic drugs, but also limits the efficacy of new biological agents. Therefore, it is important to identify the mechanisms behind chemoresistance and seek therapeutic strategies to enhance efficacy in AML chemotherapy. MicroRNA (miR)-217 has been recognized as a tumor suppressor that is downregulated in various types of cancer, however the mechanisms behind the expression and function of miR-217 in AML have not yet been recognized. The expression of miR-217 was determined by quantitative polymerase chain reaction (qPCR). Following transfection with miR-217 mimics, an MTT assay, chemosensitivity assay, cell apoptosis assay and western blot analysis were performed in AML cell lines. Functional assays were also performed to explore the effects of endogenous Kirsten rat sarcoma viral oncogene homolog (KRAS) in AML. The results revealed that miR-217 was downregulated in patients with AML. Overexpression of miR-217 inhibited cellular proliferation and enhanced cell chemosensitivity to doxorubicin by the cell apoptosis pathway in AML cells. A dual-luciferase reporter assay demonstrated that KRAS was a direct target gene of miR-217 in vitro. qPCR and western blot analysis revealed that miR-217 negatively regulated KRAS protein expression, but had no impact on KRAS mRNA expression. Knockdown of KRAS expression markedly suppressed AML cellular proliferation, and enhanced cell chemosensitivity to doxorubicin via the cell apoptosis pathway. These findings indicate that miR-217 functions as a tumor suppressor in AML by directly targeting KRAS. Therefore, miR-217-based therapeutic strategies may provide a novel strategy for the enhancement of efficacy in the treatment of AML.

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miR-217 targeting Wnt5a in osteosarcoma functions as a potential tumor suppressor

Cited by 32 publications

References 21 publications

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5

Long non‐coding RNA CRNDE promotes the proliferation, migration and invasion of hepatocellular carcinoma cells through miR‐217/MAPK1 axis

MicroRNA 217 inhibits cell proliferation and enhances chemosensitivity to doxorubicin in acute myeloid leukemia by targeting KRAS

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