In vitro effect of microRNA-107 targeting Dkk-1 by regulation of Wnt/β-catenin signaling pathway in osteosarcoma

Zhang, Zhicai; Liu, Jianxiang; Shao, Zeng-Wu; Pu, Feifei; Wang, Bai-Chuan; Wu, Qiang; Zhang, Yukun; Zeng, Xianlin; Guo, Xiaodong; Yang, Shuai; He, Tong‐Chuan

doi:10.1097/md.0000000000007245

Cited by 25 publications

(20 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some studies have also shown Wnt signalling to be neuroprotective [114, 115]. Mir-107 has been shown to regulate Dkk1; however, this was in osteosarcoma [116].…”

Section: Network Analysis Of Deregulated Mirna At Braak Stage III In mentioning

confidence: 99%

Systematic Review of miRNA as Biomarkers in Alzheimer’s Disease

et al. 2019

View full text Add to dashboard Cite

Currently there are 850,000 people with Alzheimer’s disease in the UK, with an estimated rise to 1.1 million by 2025. Alzheimer’s disease is characterised by the accumulation of amyloid-beta plaques and hyperphosphorylated tau in the brain causing a progressive decline in cognitive impairment. Small non-coding microRNA (miRNA) sequences have been found to be deregulated in the peripheral blood of Alzheimer patients. A systematic review was conducted to extract all miRNA found to be significantly deregulated in the peripheral blood. These deregulated miRNAs were cross-referenced against the miRNAs deregulated in the brain at Braak Stage III. This resulted in a panel of 10 miRNAs (hsa-mir-107, hsa-mir-26b, hsa-mir-30e, hsa-mir-34a, hsa-mir-485, hsa-mir200c, hsa-mir-210, hsa-mir-146a, hsa-mir-34c, and hsa-mir-125b) hypothesised to be deregulated early in Alzheimer’s disease, nearly 20 years before the onset of clinical symptoms. After network analysis of the 10 miRNAs, they were found to be associated with the immune system, cell cycle, gene expression, cellular response to stress, neuron growth factor signalling, wnt signalling, cellular senescence, and Rho GTPases.

show abstract

“…Some studies have also shown Wnt signalling to be neuroprotective [114, 115]. Mir-107 has been shown to regulate Dkk1; however, this was in osteosarcoma [116].…”

Section: Network Analysis Of Deregulated Mirna At Braak Stage III In mentioning

confidence: 99%

Systematic Review of miRNA as Biomarkers in Alzheimer’s Disease

et al. 2019

View full text Add to dashboard Cite

show abstract

“…In the present study, the protein expression levels of BAX, TP53 and caspase 3 were significantly increased, and those of TRIAP1 were decreased, in the miR-107 mimics group compared with the NC group. Therefore, it was hypothesized that miR-107 may induce the apoptosis of lung cancer cells by targeting TRIAP1 and increasing the expression levels of BAX, TP53 and caspase 3, which are three known tumor suppressors in lung cancer (32,33). Furthermore, previous studies have demonstrated that BCL2 knockdown decreased the viability and increased apoptosis of lung cancer cells (38), while overexpression of BCL2 decreased apoptosis of human lung cancer cells (39).…”

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

View full text Add to dashboard Cite

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.

show abstract

“…Du et al, [ 44 ] found that inhibition of miRNA- 184 may reduce tumor volume of osteosarcoma by regulating the Wnt /β- catenin signaling pathway. Zhang et al, [ 45 ] suggested that miR-107 inhibit development of osteosarcoma via the Wnt signaling pathway, and the critical role of miR- 214 in human osteosarcoma also through involving the Wnt signaling pathway. [ 46 ] Hence, it was proposed that miR-9-3p may possess a vital effect on osteosarcoma by Wnt signaling pathway.…”

Section: Discussionmentioning

confidence: 99%