Dual inhibition of PCDH9 expression by miR-215-5p up-regulation in gliomas

Wang, Chunlin; Chen, Qi; Li, Shu; Li, Shiting; Zhao, Zhenyu; Gao, Hongliang; Wang, Xiaoqiang; Li, Bin; Zhang, Wenchuan; Yuan, Yan; Ming, LinZhao; He, Hua; Tao, Bei; Zhong, Jun

doi:10.18632/oncotarget.14396

Cited by 31 publications

(28 citation statements)

References 36 publications

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“…These findings were consistent with the previous report, in which miR-215-5p inhibits the progression of colon cancer by modulating epidermal growth factor receptor ligand and Homeobox protein Hox-B9 [20]. In contrast, miR-215-5p had the potential of inhibiting the mRNA and the protein expression of Protocadherin-9 in glioma cells through regulating its promoter and 3'-UTR [21]. The luciferase reporter gene assay and western blotting assay demonstrated that Sox9 is the potential target of miR-215-5p in breast cancer.…”

Section: Discussionsupporting

confidence: 93%

miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells by targeting Sox9

Gao

Zhu

2019

FEBS Open Bio

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Several studies have shown that miR‐215‐5p acts as a tumor suppressor in certain cancers, but its role in the progression and metastasis of breast carcinoma remains incompletely understood. Herein, we prove that miR‐215‐5p is substantially down‐expressed in breast carcinoma as compared with nontumor tissue. Up‐regulation of miR‐215‐5p inhibits the aggressive abilities of breast carcinoma cells in vitro. We performed luciferase reporter tests to show that SRY‐Box 9 (Sox9) is the target of miR‐215‐5p; as predicted, Sox9 depletion replicates the suppressive effects of miR‐215‐5p on breast carcinoma cells, and overexpression of Sox9 rescues the effects of miR‐215‐5p on breast cancer cell progression. In addition, a xenograft model assay was used to reveal that miR‐215‐5p inhibits breast cancer cell growth and metastatic potential in vivo. Overall, these results imply that miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells through targeting Sox9.

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Section: Discussionsupporting

confidence: 93%

miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells by targeting Sox9

Gao

Zhu

2019

FEBS Open Bio

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“…It has been reported that miR-215-5p is a tumor suppressor in colorectal cancer and upregulation of miR-215-5p inhibited cell proliferation of glioma. 21,22 Our findings suggested that miR-215-5p expression was markedly upregulated in the BM specimens as well as cell lines of MM compared to that in HD ( Figure 1A,B), suggesting that miR-215-5p might exert a vital part in MM development. Kaplan-Meier curves indicated that there was no difference in survival rate between miR-215-5p high expression group and miR-215-5p low expression group ( Figure 1C).…”

Section: Discussionmentioning

confidence: 71%

miR‐215‐5p is an anticancer gene in multiple myeloma by targeting RUNX1 and deactivating the PI3K/AKT/mTOR pathway

Liu

Zhang

Huang

et al. 2019

J of Cellular Biochemistry

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This study examined the underlying mechanism of miR‐215‐5p in multiple myeloma (MM) at the molecular level. miR‐215‐5p was upregulated in bone marrow specimens of patients with MM and MM cell lines through real‐time polymerase chain reaction, and downregulation of miR‐215‐5p was related to poor survival of patients with MM. The results of Western blot assay showed that the PI3K/AKT/mTOR signaling pathway was activated in bone marrow specimens of patients with MM. miR‐215‐5p was found to negatively correlate with runt‐related transcription factor 1 (RUNX1) expression in MM clinical bone marrow samples. Therefore, to test the probable mechanisms of the regulation of MM cell proliferation and apoptosis, a miR‐215‐5p mimics/inhibitors/negative control was transfected into MM cells. The targets of miR‐215‐5p were estimated using four bioinformatics databases (including miRDB, miRTarBase, Starbase, and Targetscan). Furthermore, enrichment analyses of gene ontology and Kyoto Encyclopedia of Genomes pathway were carried out at the Enrichr website. Cell viability was detected using the MTT method, while apoptosis and cell cycle were measured using flow cytometry. RUNX1, CDK2, CDC25B, cleaved‐caspase‐3, cleaved‐PARP, p‐PI3K, PI3K, p‐AKT, AKT, p‐mTOR as well as mTOR protein were also investigated using Western blot analysis. According to our findings, miR‐215‐5p overexpression could induce apoptosis while rendering cell cycle arrest at G1 phase and reducing the proliferation of cells. Meanwhile, miRNA‐215‐5p could negatively regulate messengerRNA and protein levels of RUNX1 in MM cells. In addition, there was a similar effect in cell proliferation and apoptosis after miR‐215‐5p mimics or siRNA‐RUNX1 transfection. miR‐215‐5p inhibition inhibited apoptosis while increased the phosphorylation levels of PI3K, AKT, and mTOR proteins, whereas, miR‐215‐5p overexpression increased cell proliferation. Therefore, miR‐215‐5p inhibited MM cell apoptosis via targeting RUNX1 and suppressing the activation of the PI3K/AKT/mTOR pathway.

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“…PCDH9 was identified as the downstream target of miR-215-5p in gliomas and inhibited the growth of glioma cells. 35 In this study, the possible binding sites of miR-200a-3p at the 3ʹ-UTR of PCDH9 was predicted with the miRDB. Functional analysis showed that miR-200a-3p bound the 3ʹ-UTR of PCDH9 and suppressed the expression of PCDH9 in ovarian cancer cells.…”

Section: Discussionmentioning

confidence: 98%

“…Previous studies demonstrated that PCDH9 was down-regulated in cancers, such as glioblastoma, hepatocellular carcinoma and gastric cancer. [35][36][37][38] Overexpression of PCDH9 inhibited the proliferation, migration and invasion of cancer cells. However, the function of PCDH9 in ovarian cancer remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

<p>MiR-200a-3p promoted the malignant behaviors of ovarian cancer cells through regulating PCDH9</p>

Shi¹,

Yang²,

Zhang³

et al. 2019

OTT

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Background: Increasing evidence has revealed that the aberrant expression of microRNAs (miRNAs) plays vital roles in the development and progression of ovarian cancer. MiR-200a-3p was found to act as an oncogene in a variety of cancers, however, the expression and function of miR-200a-3p in ovarian cancer has not been characterized. Materials and methods: The expression of miR-200a-3p in ovarian cancer tissues and cell lines was detected by the RT-qPCR. The influence of miR-200a-3p on the growth of ovarian cancer cells was determined with the Cell Counting Kit-8 assay, colony formation and cell invasion assay. The binding of miR-200a-3p with the 3ʹ-untranslated region (UTR) of PDCH9 was detected by luciferase reporter assay. The expression of PCDH9 was investigated by RT-qPCR and Western blot analysis. Results: miR-200a-3p was up-regulated in ovarian cancer tissues and cell lines. Highly expressed miR-200a-3p was significantly associated with the tumor size, tumor metastasis and TNM stage. Overexpression of miR-200a-3p markedly promoted the proliferation, colony formation and invasion of ovarian cancer cells. Functional study uncovered that miR-200a-3p bound the 3ʹ-untranslated region (UTR) of PCDH9 and decreased the expression of PCDH9 in ovarian cancer cells. The expression of miR-200a-3p in ovarian cancer tissues was significantly negatively correlated with that of PCDH9. Restored PCDH9 inhibited the promoting effect of miR-200a-3p on the proliferation of ovarian cancer cells. Conclusion: Our results suggested the potential oncogenic function of miR-200a-3p via modulating PCDH9 in ovarian cancer.

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Dual inhibition of PCDH9 expression by miR-215-5p up-regulation in gliomas

Cited by 31 publications

References 36 publications

miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells by targeting Sox9

miRNA‐215‐5p suppresses the aggressiveness of breast cancer cells by targeting Sox9

miR‐215‐5p is an anticancer gene in multiple myeloma by targeting RUNX1 and deactivating the PI3K/AKT/mTOR pathway

<p>MiR-200a-3p promoted the malignant behaviors of ovarian cancer cells through regulating PCDH9</p>

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