Inhibitory Effect of MicroRNA-107 on Osteosarcoma Malignancy Through Regulation of Wnt/β-catenin Signaling in Vitro

Yu, Miao; Guo, Dan‐qing; Cao, Zheng-lin; Xiao, Longyi; Wang, Gang

doi:10.1080/07357907.2018.1439055

Cited by 9 publications

(9 citation statements)

References 23 publications

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“…Therefore, miR-107 acts as a tumor suppressor or oncogene in different types of cancer. The present study demonstrated that miR-107 may function as a tumor suppressor in lung cancer, which corresponds with previous studies (17)(18)(19)(20).…”

Section: Discussionsupporting

confidence: 93%

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MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

Cai

Chen

et al. 2020

Oncol Lett

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Lung cancer causes over 1.6 million mortalities worldwide annually. MicroRNAs (miRs) are involved in various types of cancer-associated processes. The present study investigated the possible mechanism of miR-107 in the development of lung cancer in order to identify novel targets for clinical treatment. The expression levels of miR-107 and its putative target gene TP53 regulated inhibitor of apoptosis 1 (TRIAP1) were measured in lung cancer tumor tissues and non-tumor adjacent tissues. Subsequently, the association between TRIAP1 and miR-107 was investigated using a dual-luciferase reporter assay. Following transfection, the effects of miR-107 and TRIAP1 on the proliferation and apoptosis of lung cancer cell lines in vitro were investigated using Cell Counting Kit-8 and flow cytometry assays, respectively. Furthermore, the regulatory effect of miR-107 on the expression levels of TRIAP1 and associated proteins was analyzed using a western blot assay. The results revealed lower expression levels of miR-107 and higher expression levels of TRIAP1 in lung cancer tumor tissues compared with non-tumor adjacent tissues. The dual-luciferase reporter assay demonstrated that TRIAP1 is a target gene of miR-107. Additionally, the results revealed that overexpression of miR-107 resulted in a lower proliferation rate and higher apoptosis rate of A549 cells, compared with the negative control (NC) and control groups (P<0.01). The variation of cell proliferation and apoptosis induced by miR-107 mimics was reversed by co-transfection with pcDNA3.1-TRIAP1. Furthermore, the expression levels of cyclin D1 and proliferating cell nuclear antigen were markedly decreased in the miR-107 mimics group compared with the NC group (P<0.01). The expression levels of BCL2 associated X apoptosis regulator, tumor protein p53 and caspase 3 were upregulated and the expression levels of TRIAP1 and BCL2 apoptosis regulator were significantly reduced in the miR-107 mimics group compared with the NC group (P<0.01). The results of the present study suggested that miR-107 regulates lung cancer cell proliferation and apoptosis by targeting TRIAP1.

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Section: Discussionsupporting

confidence: 93%

“…Furthermore, miR-107 promoted the proliferation and invasion of gastric adenocarcinoma cells through large tumor suppressor kinase 2 (18). However, miR-107 inhibited cell proliferation and metastasis in gastric cancer (19) and osteosarcoma (20). Therefore, miR-107 acts as a tumor suppressor or oncogene in different types of cancer.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

Cai

Chen

et al. 2020

Oncol Lett

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“…Various miRNAs play a significant role in atherogenesis (Quiat & Olson, ). The role of miR‐107 in several cancers as cell proliferative suppressor and apoptotic promoter has been largely investigated (J. Chen et al, ; Yu, Guo, Cao, Xiao, & Wang, ). This study illustrated the regulatory role and mechanism of miR‐107 in coronary atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

microRNA‐107 protects against inflammation and endoplasmic reticulum stress of vascular endothelial cells via KRT1‐dependent Notch signaling pathway in a mouse model of coronary atherosclerosis

Gao

et al. 2018

Journal Cellular Physiology

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Coronary atherosclerosis is a long‐term, sustained, and evolving inflammatory disease manifested with the remodeling of the coronary arteries. The purpose of this study is to explore the potential role of microRNA‐107 (miR‐107) in vascular endothelial cells (VECs) in coronary atherosclerosis by regulating the KRT1 gene and the Notch signaling pathway. A mouse model of coronary atherosclerosis was established. The relationship between miR‐107 and KRT1 was analyzed and verified by dual‐luciferase reporter assay. The functional role of miR‐107 in coronary atherosclerosis was determined using ectopic expression and depletion. Blood lipid levels and atherosclerotic index (AI) were measured in atherosclerotic mice. Expression pattern of miR‐107, KRT1, Notch signaling pathway, inflammatory/anti‐inflammatory factors, and endoplasmic reticulum (ER) stress‐related genes was evaluated by means of reverse transcription quantitative polymerase chain reaction, western blot analysis, and enzyme‐linked immunosorbent assay. Meanwhile, cell‐cycle distribution and cell apoptosis in VECs were assessed by flow cytometry. Atherosclerotic mice exhibited higher blood lipid levels, AI, apoptotic index, and KRT1‐positive expression as well as inhibited Notch signaling pathway when compared with normal mice. The miR‐107 was revealed to bind to KRT1; miR‐107 upregulation or KRT1 silencing resulted in reductions in blood lipid levels and AI, inhibition in cell apoptosis, inflammation, and ER stress. Restored miR‐107 or downregulated KRT1 activated the Notch signaling pathway. These results supported the notion that miR‐107‐targeted KRT1 inhibition activated the Notch pathway, thereby, protecting against the coronary atherosclerosis. Findings in this study might provide a novel biomarker for the coronary atherosclerosis treatment.

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“…In addition, the Wnt/β-catenin signaling pathway was reported to be activated in OS tissues and cells, and aberrant activation may serve a central role in the tumorigenesis, metastasis and chemotherapeutic responses of OS (31,32). Numerous reports have revealed that microRNAs regulate the Wnt signaling pathway in OS (33)(34)(35), indicating that microRNAs may be the upstream molecules involved in FOXN3 signaling.…”

Section: Discussionmentioning

confidence: 99%

FOXN3 is downregulated in osteosarcoma and transcriptionally regulates SIRT6, and suppresses migration and invasion in osteosarcoma

Xue

Wang

et al. 2018

Oncol Rep

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Forkhead box N3 (FOXN3) has been reported to be downregulated in numerous cancers, including laryngeal, oral squamous cell and hepatocellular carcinomas, and diffuse large B-cell lymphoma. FOXN3 was proposed to serve as a tumor suppressor; however, the function of FOXN3 in osteosarcoma (OS) remains unknown. The present study suggested that FOXN3 was notably downregulated in OS tissues compared with in adjacent normal tissues, and the expression of FOXN3 was negatively correlated with tumor size, metastasis and tumor, node and metastasis stage. Additionally, low expression levels of FOXN3 predicted a poor prognosis of patients with OS. Additionally, the present study revealed that FOXN3 was also downregulated in OS cells. Numerous functional experiments, including colony formation, Cell Counting Kit-8, wound healing and Transwell invasion assays, were performed. The results of the present study revealed that FOXN3 suppressed the proliferation, migration and invasion of OS cells. SIRT6 has been reported to serve a key role in OS; chromatin-immunoprecipitation (ChIP) and quantitative ChIP, as well as a luciferase reporter assay, demonstrated that SIRT6 was transcriptionally regulated by FOXN3. Furthermore, FOXN3 also regulated matrix metalloproteinase-9 secretion via the regulation of SIRT6 expression. The findings of the present study indicated that FOXN3 serves as a tumor suppressor in OS and proposed FOXN3 as a prognostic predictor and a therapeutic target for patients with OS.

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Inhibitory Effect of MicroRNA-107 on Osteosarcoma Malignancy Through Regulation of Wnt/β-catenin Signaling in Vitro

Cited by 9 publications

References 23 publications

MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

MicroRNA‑107 may regulate lung cancer cell proliferation and apoptosis by targeting TP53 regulated inhibitor of apoptosis 1

microRNA‐107 protects against inflammation and endoplasmic reticulum stress of vascular endothelial cells via KRT1‐dependent Notch signaling pathway in a mouse model of coronary atherosclerosis

FOXN3 is downregulated in osteosarcoma and transcriptionally regulates SIRT6, and suppresses migration and invasion in osteosarcoma

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