miR‑145 inhibits human non‑small-cell lung cancer growth by dual-targeting RIOK2 and NOB1

K, Liu; Chen, Honglin; You, Qingsheng; Ye, Qing; Wang, Fei; Wang, Shuo; Zhang, Shuanglong; Yu, Kang-Jun; Li, Weinan; Gu, Ming

doi:10.3892/ijo.2018.4393

Cited by 15 publications

(18 citation statements)

References 39 publications

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“…NOB1 was reportedly linked to the onset and development of various tumours and plays the role of an oncogene . A previous study showed that NOB1 levels were elevated in cervical cancer tissues and cell lines .…”

Section: Discussionmentioning

confidence: 99%

“…21,22 NOB1 was reportedly linked to the onset and development of various tumours and plays the role of an oncogene. [23][24][25][26][27] A previous study showed that NOB1 levels were elevated in cervical cancer tissues and cell lines. 28 Studies have also demonstrated that miR-139-3p inhibited cervical cancer cell proliferation, migration, and invasion and induced cell apoptosis through down-regulation of NOB1 expression.…”

Section: Discussionmentioning

confidence: 99%

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RETRACTED: MicroRNA‐612 inhibits cervical cancer progression by targeting NOB1

Yang

Zhou

Yao

et al. 2020

J Cellular Molecular Medi

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Recently, many studies have shown that microRNA (miR)‐612 is involved in cancer progression. However, the role of miR‐612 in cervical cancer remains unclear. The present study aims to investigate the biological effects of miR‐612 on cervical cancer. The expression of miR‐612 in cervical cancer tissues and cell lines was analysed by quantitative reverse transcription‐polymerase chain reaction. The effect of miR‐612 cell proliferation, migration, invasion and apoptosis was studied by appropriate methods. Protein expression was determined by Western blot analyses. Bioinformatics analysis and luciferase reporter assays were performed to clarify the relationship between miR‐612 and nin one binding protein (NOB1). A xenograft model was established to examine the role of miR‐612 in vivo tumorigenesis. Cervical cancer tissues and cell lines showed down‐regulation of miR‐612 expression, which was associated with the Fédération Internationale de Gynécologie et d'Obstétrique (FIGO) stage and lymph node metastasis. Functional assays revealed that miR‐612 overexpression significantly suppressed cervical cancer cell proliferation, migration and invasion in vitro and delayed tumour growth in vivo. Mechanically, miR‐612 targeted NOB1 in cervical cancer cells, revealing a negative correlation between miR‐612 and NOB1in cervical cancer samples. NOB1 overexpression partially reversed the inhibitory effects of miR‐612 overexpression in cervical cancer cells. Taken together, these findings indicate that miR‐612 functions as a tumour suppressor in cervical cancer and suggest that miR‐612 may be a potential target in the therapeutic intervention of this malignancy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

RETRACTED: MicroRNA‐612 inhibits cervical cancer progression by targeting NOB1

Yang

Zhou

Yao

et al. 2020

J Cellular Molecular Medi

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“…MiRNAs affect biological behaviours such as tumour occurrence, proliferation and invasion mostly by regulating target genes. It has been reported that miR‐145 inhibits non‐small‐cell lung cancer growth by targeting RIOK2 31 . NeuroD2 is post‐transcriptionally targeted by miR‐210, overexpression of NeuroD2 diminishes glioma cell proliferation, migration, and promotes apoptosis under hypoxia 18 .…”

Section: Discussionmentioning

confidence: 99%

RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

Song

Cheng

Jin

et al. 2020

J Cellular Molecular Medi

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RIOK2 is a member of RIO (right open reading frame) kinase family. Recent studies have revealed the involvement of RIO kinases in glioma cell growth and expansion. However, the role and mechanism of RIOK2 in glioma cell migration and invasion remain unclear. Wound healing assay, Transwell assay and real-time quantitative PCR (qRT-PCR) detection of matrix metalloproteinases (MMPs) were used to evaluate the migration/invasion of glioma cells. Western blot and qRT-PCR were employed to measure the expression of epithelial-mesenchymal transition (EMT) markers. Dual luciferase reporter assay was performed to determine the binding between RIOK2 and miR-4744. In addition, RIOK2 and miR-4744 levels were quantified by qRT-PCR and/ or immunohistochemistry in glioma tissues. Transfection of RIOK2 siRNAs significantly inhibited glioma cell migration and invasion and down-regulated the expression of MMPs (MMP2 and MMP9) and mesenchymal markers (N-cadherin, β-catenin, Twist1, fibronectin, ZEB-1) in glioma cells. Overexpression of RIOK2 showed the opposite effects. MiR-4744 directly bound to the 3'-untranslated region of RIOK2 and negatively regulated the expression of RIOK2. Up-regulation of miR-4744 inhibited the migration and invasion of glioma cells. Overexpression of RIOK2 could reverse the effects of miR-4744 up-regulation on the migration, invasion and EMT process in glioma cells. Moreover, RIOK2 was high, while miR-4744 was low in glioma tissues, and a negative correlation was found between them. These results suggest that RIOK2 is post-transcriptionally targeted by miR-4744, the low miR-4744 and high RIOK2 levels in glioma may contribute to tumour cell infiltration through promoting the EMT. K E Y W O R D S fibronectin, glioma, miR-4744, N-cadherin, RIOK2, β-catenin | 4495 SONG et al. S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section. How to cite this article: Song Y, Li C, Jin L, et al. RIOK2 is negatively regulated by miR-4744 and promotes glioma cell migration/invasion through epithelial-mesenchymal transition.

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“…EMNs were loaded with therapeutic miR-145 labelled with the fluorescent tag, Cy-5. MiR-145 is a potent tumor-suppressor downregulated in lung cancer and known to inhibit right open reading frame kinase 2 (RIOK2) and NIN1 binding protein (NOB1) [54]. After IP injection of the ENM-miR-145-Cy-5, a fluorescent signal was detected at the lung tumor sites.…”

Section: Tumor Suppressive Mirna Delivery Via Extracellular Vesicles mentioning

confidence: 99%

Nanoparticle-Based Delivery of Tumor Suppressor microRNA for Cancer Therapy

O'Neill

Dwyer

2020

Cells

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Improved understanding of microRNA expression and function in cancer has revealed a range of microRNAs that negatively regulate many oncogenic pathways, thus representing potent tumor suppressors. Therapeutic targeting of the expression of these microRNAs to the site of tumors and metastases provides a promising avenue for cancer therapy. To overcome challenges associated with microRNA degradation, transient expression and poor targeting, novel nanoparticles are being developed and employed to shield microRNAs for tumor-targeted delivery. This review focuses on studies describing a variety of both natural and synthetic nanoparticle delivery vehicles that have been engineered for tumor-targeted delivery of tumor suppressor microRNAs in vivo.

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miR‑145 inhibits human non‑small-cell lung cancer growth by dual-targeting RIOK2 and NOB1

Cited by 15 publications

References 39 publications

RETRACTED: MicroRNA‐612 inhibits cervical cancer progression by targeting NOB1

RETRACTED: MicroRNA‐612 inhibits cervical cancer progression by targeting NOB1

RIOK2 is negatively regulated by miR‐4744 and promotes glioma cell migration/invasion through epithelial‐mesenchymal transition

Nanoparticle-Based Delivery of Tumor Suppressor microRNA for Cancer Therapy

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