<scp>miRNA‐10a‐5p</scp> inhibits cell metastasis in hepatocellular carcinoma via targeting <scp>SKA1</scp>

Shen, Duo; Zhao, Hongyu; Gu, Aidong; Wu, Yin-Wei; Weng, Yu-Hang; Li, Shujie; Song, Jinyun; Gu, Xuefeng; Qiu, Jie; Zhao, Wei

doi:10.1002/kjm2.12392

Cited by 15 publications

(6 citation statements)

References 27 publications

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“…These relationships provide a potential mechanism on how this lncRNA contributes to the downregulation of mRNAs ( Table 2 ). In the s iOCT4-POVPC vs. siOCT4-DMSO groups, downregulated ENSMUST00000173605 had three predicted binding sites for mmu-miR-10a-5p/mmu-miR-10b-5p, and two predicted sites for mmu-miR-15a-5p/mmu-miR-15b-5p and mmu-miR-30a-5p (all upregulated miRNAs), which were reported to regulate cell migration and apoptosis ( Shen et al, 2021 ; Li et al, 2022 ; Chen et al, 2020 ), and phagocytosis ( Cho et al, 2019 ; Murinello et al, 2019 ) and were associated with downregulated mRNAs ( Table 2 ).…”

Section: Resultsmentioning

confidence: 99%

Integrative analysis of the lncRNA-miRNA-mRNA interactions in smooth muscle cell phenotypic transitions

Mahajan,

Hong,

Krukovets

et al. 2024

Front. Genet.

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Objectives: We previously found that the pluripotency factor OCT4 is reactivated in smooth muscle cells (SMC) in human and mouse atherosclerotic plaques and plays an atheroprotective role. Loss of OCT4 in SMC in vitro was associated with decreases in SMC migration. However, molecular mechanisms responsible for atheroprotective SMC-OCT4-dependent effects remain unknown.Methods: Since studies in embryonic stem cells demonstrated that OCT4 regulates long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), making them candidates for OCT4 effect mediators, we applied an in vitro approach to investigate the interactions between OCT4-regulated lncRNAs, mRNAs, and miRNAs in SMC. We used OCT4 deficient mouse aortic SMC (MASMC) treated with the pro-atherogenic oxidized phospholipid POVPC, which, as we previously demonstrated, suppresses SMC contractile markers and induces SMC migration. Differential expression of lncRNAs, mRNAs, and miRNAs was obtained by lncRNA/mRNA expression array and small-RNA microarray. Long non-coding RNA to mRNA associations were predicted based on their genomic proximity and association with vascular diseases. Given a recently discovered crosstalk between miRNA and lncRNA, we also investigated the association of miRNAs with upregulated/downregulated lncRNA-mRNA pairs.Results: POVPC treatment in SMC resulted in upregulating genes related to the axon guidance and focal adhesion pathways. Knockdown of Oct4 resulted in differential regulation of pathways associated with phagocytosis. Importantly, these results were consistent with our data showing that OCT4 deficiency attenuated POVPC-induced SMC migration and led to increased phagocytosis. Next, we identified several up- or downregulated lncRNA associated with upregulation of the specific mRNA unique for the OCT4 deficient SMC, including upregulation of ENSMUST00000140952-Hoxb5/6 and ENSMUST00000155531-Zfp652 along with downregulation of ENSMUST00000173605-Parp9 and, ENSMUST00000137236-Zmym1. Finally, we found that many of the downregulated miRNAs were associated with cell migration, including miR-196a-1 and miR-10a, targets of upregulated ENSMUST00000140952, and miR-155 and miR-122, targets of upregulated ENSMUST00000155531. Oppositely, the upregulated miRNAs were anti-migratory and pro-phagocytic, such as miR-10a/b and miR-15a/b, targets of downregulated ENSMUST00000173605, and miR-146a/b and miR-15b targets of ENSMUST00000137236.Conclusion: Our integrative analyses of the lncRNA-miRNA-mRNA interactions in SMC indicated novel potential OCT4-dependent mechanisms that may play a role in SMC phenotypic transitions.

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Section: Resultsmentioning

confidence: 99%

Integrative analysis of the lncRNA-miRNA-mRNA interactions in smooth muscle cell phenotypic transitions

Mahajan,

Hong,

Krukovets

et al. 2024

Front. Genet.

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“…In recent years, a growing number of miRNAs associated with HCC have been successively confirmed. Shen et al experimentally proved that miRNA-10a-5p acted on SKA1 to inhibit the metastasis of hepatocellular carcinoma cells [ 22 ]. Liu et al demonstrated that miRNA-494 can promote cell proliferation in HCC [ 23 ].…”

Section: Resultsmentioning

confidence: 99%

TLNPMD: Prediction of miRNA-Disease Associations Based on miRNA-Drug-Disease Three-Layer Heterogeneous Network

et al. 2022

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Many microRNAs (miRNAs) have been confirmed to be associated with the generation of human diseases. Capturing miRNA–disease associations (M-DAs) provides an effective way to understand the etiology of diseases. Many models for predicting M-DAs have been constructed; nevertheless, there are still several limitations, such as generally considering direct information between miRNAs and diseases, usually ignoring potential knowledge hidden in isolated miRNAs or diseases. To overcome these limitations, in this study a novel method for predicting M-DAs was developed named TLNPMD, highlights of which are the introduction of drug heuristic information and a bipartite network reconstruction strategy. Specifically, three bipartite networks, including drug–miRNA, drug–disease, and miRNA–disease, were reconstructed as weighted ones using such reconstruction strategy. Based on these weighted bipartite networks, as well as three corresponding similarity networks of drugs, miRNAs and diseases, the miRNA–drug-disease three-layer heterogeneous network was constructed. Then, this heterogeneous network was converted into three two-layer heterogeneous networks, for each of which the network path computational model was employed to predict association scores. Finally, both direct and indirect miRNA–disease paths were used to predict M-DAs. Comparative experiments of TLNPMD and other four models were performed and evaluated by five-fold and global leave-one-out cross validations, results of which show that TLNPMD has the highest AUC values among those of compared methods. In addition, case studies of two common diseases were carried out to validate the effectiveness of the TLNPMD. These experiments demonstrate that the TLNPMD may serve as a promising alternative to existing methods for predicting M-DAs.

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“…MMP3 is regulated by various miRNAs [18,19], subsequently facilitating tumor cell invasion and metastasis [15][16][17]. The abnormal expression of miRNAs has been closely associated with processes such as tumor cell invasion and metastasis in osteosarcoma [18,19,[52][53][54]. For example, the increased expression of MMP-3 induces tumor metastasis in osteosarcoma by inhibiting miR-519d [19], and miR-134 reduces osteosarcoma cell invasion and metastasis by targeting MMP-3 in vivo and in vitro [18].…”

Section: Discussionmentioning

confidence: 99%

Chemokine Ligand 2 Promotes Migration in Osteosarcoma by Regulating the miR-3659/MMP-3 Axis

Chang,

Huang,

Tsai

et al. 2023

Biomedicines

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Osteosarcoma is a common malignant tumor in children and adolescents, known for its aggressive invasion and distant metastasis, leading to a poor prognosis. Matrix metalloproteinases (MMPs) can degrade the extracellular matrix and basement membranes through their proteolytic activity, thereby promoting osteosarcoma metastasis. Chemokine ligand 2 (CCL2) is a well-studied chemokine that plays a significant role in the cell motility of many cancers. However, its specific involvement in osteosarcoma metastasis is not fully understood. The aim of this study is to examine the role of miRNAs in CCL2-mediated MMP expression and cell motility in human osteosarcoma. The analysis of immunohistochemistry data and databases associated a positive correlation between CCL2 or MMP-3 levels with the metastasis of osteosarcoma patients. The in vivo lung metastatic osteosarcoma model also demonstrated similar effects, showing higher levels of CCL2 and MMP-3 in lung metastatic osteosarcoma tissues. The stimulation of osteosarcoma cells with CCL2 enhanced migration and invasion abilities through the upregulation of MMP-3 synthesis. Our results also indicate that CCL2 enhances MMP-3-dependent cell motility by inhibiting miR-3659 synthesis. Therefore, CCL2 represents a promising therapeutic target for treating metastasis in osteosarcoma.

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miRNA‐10a‐5p inhibits cell metastasis in hepatocellular carcinoma via targeting SKA1

Cited by 15 publications

References 27 publications

Integrative analysis of the lncRNA-miRNA-mRNA interactions in smooth muscle cell phenotypic transitions

Integrative analysis of the lncRNA-miRNA-mRNA interactions in smooth muscle cell phenotypic transitions

TLNPMD: Prediction of miRNA-Disease Associations Based on miRNA-Drug-Disease Three-Layer Heterogeneous Network

Chemokine Ligand 2 Promotes Migration in Osteosarcoma by Regulating the miR-3659/MMP-3 Axis

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