&lt;p&gt;LINC00963 Functions as an Oncogene in Bladder Cancer by Regulating the miR-766-3p/MTA1 Axis&lt;/p&gt;

Zhou, Ning; Zhu, Xiaofei; Man, Libo

doi:10.2147/cmar.s249979

Cited by 18 publications

(10 citation statements)

References 30 publications

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“…miRNAs are also identified important in the progression of OS by regulating cell proliferation, EMT, and metastasis ( Leichter et al, 2017 ; Fellenberg et al, 2019 ; Luo et al, 2019 ; Zhang K. et al, 2020 ). miR-766-3p, a tumor suppressor microRNA, is reported to down-regulated in several types of tumor, was remarkably correlated with poor clinical outcomes ( Liu et al, 2020 ; Zhou et al, 2020 ). Nevertheless, to date, there has been no detailed investigations into the functions of miR-766-3p, and the underling mechanisms is far from being fully understood in OS.…”

Section: Introductionmentioning

confidence: 99%

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Zhang

Chen

Liu

et al. 2020

Front. Cell Dev. Biol.

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Accumulating evidence has indicated that abnormal microRNAs (miRNAs) serve critical roles in carcinogenesis and development of osteosarcoma (OS). The purpose of the present study was to elucidate the relationship between miR-766-3p and development of osteosarcoma and explore the potential mechanism. In this study, we found that miR-766-3p was the most downregulated miRNA by analyzing GSE65071 from the GEO database. miR-766-3p was lowly expressed in OS tissue samples and cells, and high miR-766-3p expression repressed the malignant level of OS, including cell proliferation, EMT, migration, and invasion in vitro and in vivo. B-Cell Lymphoma 9-Like Protein (BCL9L) was negatively associated with miR-766-3p expression in OS cells and tissue samples and was validated as the downstream target by luciferase reporter assay and western blotting. Rescue experiment indicated that BCL9L could restore the influence of miR-766-3p on OS cells. In addition, the β-Catenin/TCF-4 signal pathway was demonstrated to be related to the miR-766-3p/BCL9L axis. In summary, miR-766-3p, a negative regulator of BCL9L, plays the role of tumor metastasis suppressor via the β-catenin signaling pathway in the progression of OS.

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Section: Introductionmentioning

confidence: 99%

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Zhang

Chen

Liu

et al. 2020

Front. Cell Dev. Biol.

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“…LINC00963 also conferred oncogenic properties in bladder cancer as high LINC00963 expression was observed in bladder cancer patients and indicated high histological grade. Bladder cancer cells viability, colony formation, migration, and invasion can be suppressed by LINC00963 knocking down [ 16 ]. In our study, LINC00963 was found to have a significant high expression level in breast cancer patients in TCGA database.…”

Section: Discussionmentioning

confidence: 99%

Corylin suppresses metastasis of breast cancer cells by modulating miR-34c/LINC00963 target

Liu¹,

Wang

Zhang³

2021

Libyan Journal of Medicine

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Breast cancer is one of the cancers leading to most death cases among women and metastasis is the major cause of breast cancer mortality. In this study, Corylin, the flavonoid compound which is extracted and purified from Psoralea corylifolia L., the effect on breast cancer metastasis was investigated. Corylin showed inhibitory effect on migration and invasion abilities of breast cancer cells. Meanwhile, the epithelial-mesenchymal transition was also regulated by corylin. The long non-coding RNA LINC00963 was found to have a significantly high expression level in breast cancer while it can be down-regulated by corylin. In addition, both wound-healing assay and transwell assay showed that LINC00963 induced breast cancer cells metastasis. MiR-34c was increased by corylin treatment depending on p53, and it was firstly identified that the LINC00963 was a direct target of miR-34c. Corylin was verified here that it prohibited MCF-7 migration and invasion depending on miR-34c/LINC00963 target. In conclusion, corylin suppresses metastasis of breast cancer cells via increasing miR-34c expression, which was dependent on p53. LINC00963 was a direct target of miR-34c and the target axis was necessary for corylin function. Therefore, corylin is a promising drug candidate and LINC00963 can be seen as a promising target in breast cancer treatment ARTICLE HISTORY

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“…LINC00963 has recently been reported to promote breast and hepatocellular carcinogenesis ( 22 , 23 ). Its expression is upregulated in several types of cancer, such as melanoma and bladder cancer ( 24 , 25 ). However, the association between LINC00963 and diabetes has not been reported to date.…”

Section: Discussionmentioning

confidence: 99%

LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b

et al. 2021

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The association between long intergenic non-protein-coding RNA 963 (LINC00963) and diabetes has not been fully elucidated. Therefore, the present study aimed to investigate the effect of the long non-coding RNA LINC00963 on diabetic retinopathy (DR), in order to provide a new therapeutic target for this condition. Human retinal capillary endothelial cells (HRECs) were induced with high concentrations of glucose to establish a DR model. The expression levels of LINC00963, cell viability, the protein expression levels of proliferating cell nuclear antigen (PCNA) and Ki67, and the migratory capacity of HRECs were determined using reverse transcription-quantitative PCR (RT-qPCR), Cell Counting Kit-8 assay, western blot analysis, and wound healing and Transwell assays, respectively. Furthermore, the Encyclopedia of RNA Interactomes database was used to predict the binding targets of LINC00963, and luciferase reporter assay was used to verify the direct binding of microRNA (miR)-27b to LINC00963. RT-qPCR was also utilized to measure the expression levels of miR-27b, PCNA and Ki67. The results demonstrated that LINC00963 silencing inhibited glucose-induced HREC proliferation and migration, and downregulated PCNA and Ki67 expression. Following transfection with miR-27b inhibitor, cell proliferation and migration were notably enhanced, and the protein expression levels of PCNA and Ki67 were increased. Taken together, the results of the present study suggested that the LINC00963/miR-27b axis may regulate the proliferation and migration of glucose-induced HRECs. Therefore, LINC00963 may be considered as a potential therapeutic target for DR.

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<p>LINC00963 Functions as an Oncogene in Bladder Cancer by Regulating the miR-766-3p/MTA1 Axis</p>

Cited by 18 publications

References 30 publications

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

miR-766-3p Targeting BCL9L Suppressed Tumorigenesis, Epithelial-Mesenchymal Transition, and Metastasis Through the β-Catenin Signaling Pathway in Osteosarcoma Cells

Corylin suppresses metastasis of breast cancer cells by modulating miR-34c/LINC00963 target

LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b

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