LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

Zhang, Chunyan; Xie, Linsen; Liang, Huiling; Cui, Yuanbo

doi:10.1002/iub.2001

Cited by 25 publications

(22 citation statements)

References 36 publications

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“…Thus, investigating the crosstalk between lncRNAs and miRNAs will be helpful for improving our understanding of lncRNAs. To date, several miRNAs have been reported to be sponged by MIAT, including miR-149-5p [30], miR-150-5p [31], miR-128-3p [32], and miR-29c [33]. Of note, miR-132, a key miRNA involved in chondrogenic differentiation [17], was also found to be sponged by MIAT in colorectal cancer cells [20].…”

Section: Discussionmentioning

confidence: 99%

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Song

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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The over-expanding role of lncRNA myocardial infarction associated transcript (MIAT) in various human diseases has been recently revealed. This study attempted to see the role of MIAT in a cell model of osteoarthritis (OA). ATDC5 cells were subjected to lipopolysaccharides (LPS) to mimic a cell model of OA. The effects of MIAT on the model were tested by performing CCK-8 assay, flow cytometry, qRT-PCR, western blot and ELISA. The downstream miRNA and signalling pathways were studied by utilizing qRT-PCR and western blot. Transfection of ATDC5 cells with the shRNA specific against MIAT significantly attenuated LPS-evoked apoptosis and cytokines release. At the meantime, the viability loss and the cleavage of caspases were ameliorated as well. MIAT overexpressed lead to the opposite result. Further, miR-132 was found to be negatively regulated by MIAT. The protective effects of MIAT silence were flattened when miR-132 expression was suppressed. Besides that the inhibitory effects of MIAT silence on LPS-evoked NF-jB and JNK activation were eliminated by miR-132 silence. This study illustrated that silence of MIAT protected ATDC5 cells against LPS challenge. The chondroprotective effects of MIAT silence may be via up-regulation of miR-132 and inhibition of NF-jB and JNK pathways.

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Section: Discussionmentioning

confidence: 99%

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Song

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…These results were further supported by the colony formation assays, which indicated that miat knockdown significantly inhibited the HCC cells colony formation (Figure 2G, 2H and Supplementary Figure 1Q, 1R). It has been reported that miat was associated with metastasis of solid tumors [30]. Therefore, we conducted the migration ability of miat by Transwell and Wound-healing assays.…”

Section: Resultsmentioning

confidence: 99%

lncRNA miat functions as a ceRNA to upregulate sirt1 by sponging miR-22-3p in HCC cellular senescence

Zhao

Cao

et al. 2019

Aging

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Hepatocellular carcinoma (HCC) is a leading cause of cancer related deaths and lacks effective therapies. Cellular senescence acts as a barrier against cancer progression and plays an important role in tumor suppression. Senescence associated long noncoding RNAs (SAL-RNAs) are thought to be critical regulators of cancer development. Here, the long noncoding RNA (lncRNA) myocardial infarction-associated transcript (miat) was first identified as an HCC specific SALncRNA. Knockdown of miat significantly promoted cellular senescence and inhibited HCC progression. Mechanistic study revealed that SAL-miat acted as a competitive endogenous RNA (ceRNA) that upregulated the expression of sirt1 by sponging miR-22-3p. Moreover, miat downregulation activated the tumor suppressor pathway (p53/p21 and p16/pRb) and stimulated senescent cancer cells to secrete senescence-associated secretory phenotype (SASP), which contributed to inhibition of tumor cell proliferation, and resulted in the suppression of HCC tumorigenesis. Together, our study provided mechanistic insights into a critical role of miat as a miRNA sponge in HCC cellular senescence, which might offer a potential therapeutic strategy for HCC treatment.

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“…So, the precious results and our present study demonstrated lnc-SNHG16 could be target for prevention and therapeutics for CC in future. miR-128 was low expression in osteosarcoma [24], glioma [25], ovarian cancer [26], thyroid cancer [27], HCC [28], CRC [29], gastric carcinoma (GC) [30]. However, the role and mechanism of miR-128 remains unclear in CC.…”

Section: Discussionmentioning

confidence: 99%

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

Guo²,

Liang

et al. 2020

J. Cancer

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Background: The lnc-SNHG16 serves as an oncogene and miR-128 acts as a tumor suppressor in various cancers. However, the functional role of lnc-SNHG16 and miR-128 in CC still remain unknown. This study aims to explore the expression level of lnc-SNHG16 and miR-128 and its biological roles in CC. Methods: lnc-SNHG16, miR-128, GSPT1 and WNT3A expression were analyzed using quantitative real-time PCR and bioinformatics in cervical cancer tissues and cells. Cell Counting Kit-8, EdU staining, colony formation assay, western blot, Transwell, immunofluorescence, immunohistochemical staining, luciferase reporter assay, electrophoretic mobility shift, tumor xenograft, and flow cytometry assays were employed to investigate the mechanisms underlying the effect of Lnc-SNHG16/miR-128 axis on cervical cancer. Results: lnc-SNHG16 was up-regulated in CC cell lines and tissues. lnc-SNHG16 knockdown inhibited proliferation, restrained the epithelial-mesenchymal transition (EMT) process by regulating cell apoptosis and cell cycle. The next study indicated that lnc-SNHG16 knockdown markedly increased miR-128 level which is down-regulated in CC. Moreover, miR-128 overexpression significantly inhibited proliferation, EMT process and tumor growth by directly targeting GSPT1 and WNT3A. Finally, lnc-SNHG16 activates but miR-128 inactivates the WNT/β-catenin pathways in CC cells. Conclusion: Our data suggest that lnc-SNHG16/miR-128 axis modulates malignant phenotype of CC cells through WNT/β-catenin pathway.

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LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

Cited by 25 publications

References 36 publications

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

lncRNA miat functions as a ceRNA to upregulate sirt1 by sponging miR-22-3p in HCC cellular senescence

Lnc-SNHG16/miR-128 axis modulates malignant phenotype through WNT/β-catenin pathway in cervical cancer cells

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