LncRNA XIST/miR-34a axis modulates the cell proliferation and tumor growth of thyroid cancer through MET-PI3K-AKT signaling

Liu, Hua; Deng, Hongbin; Zhao, Yajie; Li, Can; Liang, Yu

doi:10.1186/s13046-018-0950-9

Cited by 251 publications

(191 citation statements)

References 41 publications

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“…Protein samples were separated by SDS‐PAGE, transferred from gel to a PVDF membrane. The membrane was incubated with antibodies against KRT6, KRT10 and Tp63 following the methods described previously . After incubating with the primary antibodies mentioned above, the blots were incubated for 1 hour with HRP‐conjugated goat anti‐mouse or goat anti‐rabbit IgG (Beyotime).…”

Section: Methodsmentioning

confidence: 99%

Ozone therapy promotes the differentiation of basal keratinocytes via increasing Tp63‐mediated transcription of KRT10 to improve psoriasis

Gao

Dou

Zhang

et al. 2020

J Cellular Molecular Medi

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Psoriasis is a chronic immune-mediated inflammatory dermatosis. Recently, ozone therapy has been applicated to psoriasis treatment; however, the mechanism by which ozone therapy improves psoriasis remains unclear. The excessive proliferation and the differentiation of basal keratinocytes have been considered critical issues during pathological psoriasis process, in which keratin 6 (KRT6) and KRT10 might be involved. In the present study, KRT6, IL-17 and IL-22 protein within psoriasis lesions was decreased, while KRT10 and Tp63 protein in psoriasis lesions was increased by ozone treatment in both patient and IMQ mice psoriatic tissues. In the meantime, ozone treatment down-regulated KRT6 mRNA and protein expression while up-regulated KRT10 mRNA and protein expression within IL-22 treated primary KCs; the cell viability of KCs was suppressed by ozone treatment. Moreover, Tp63 bound to KRT10 promoter region to activate its transcription in basal keratinocytes; the promotive effects of ozone on Tp63 and KRT10 were significantly reversed by Tp63 silence. Both TP63 and KRT10 mRNA expression were significantly increased by ozone treatment in psoriasis lesions; there was a positive correlation between Tp63 and KRT10 expression within tissue samples, suggesting that ozone induces the expression of Tp63 to enhance the expression of KRT10 and the differentiation of keratinocytes, therefore improving the psoriasis. In conclusion, the application of ozonated oil could be an efficient and safe treatment for psoriasis; ozone promotes the differentiation of keratinocytes via increasing Tp63-mediated transcription of KRT10, therefore improving psoriasis.

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Section: Methodsmentioning

confidence: 99%

Ozone therapy promotes the differentiation of basal keratinocytes via increasing Tp63‐mediated transcription of KRT10 to improve psoriasis

Gao

Dou

Zhang

et al. 2020

J Cellular Molecular Medi

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“…The dysregulation of lncRNA expression which acted as oncogenes or tumor-suppressor genes have great significance for the occurrence, development, metastasis, clinical stage and prognosis of thyroid cancer (7)(8)(9). OTUD6B-AS1 was first reported in systemic sclerosis (10).…”

Section: Discussionmentioning

confidence: 99%

“…LncRNAs are involved in the regulatory network of thyroid carcinomas. Several lncRNAs have been reported to promote or inhibit proliferation, migration, invasion, and angiogenesis of thyroid carcinomas (7,8). In addition, dysregulation of lncRNAs is associated with poor prognoses thyroid carcinomas (9).…”

Section: Introductionmentioning

confidence: 99%

OTUD6B-AS1 Inhibits Viability, Migration, and Invasion of Thyroid Carcinoma by Targeting miR-183-5p and miR-21

et al. 2020

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Background: The long noncoding RNA (lncRNA) functions as a regulator of initiation, progression, and metastasis of thyroid carcinomas. lncRNA OTUD6B antisense RNA 1 (OTUD6B-AS1) is a tumor-suppressive noncoding RNA in clear cell renal cell carcinoma. The role of OTUD6B-AS1 in thyroid carcinomas has not been reported yet. We aim to investigate the expression and biological functions of OTUD6B-AS1 in thyroid carcinomas. Methods:The expression level of OTUD6B-AS1 was measured in 60 paired human thyroid carcinoma tissues and corresponding adjacent normal thyroid tissues. The correlations between the OTUD6B-AS1 expression levels and clinicopathological features were evaluated using the Mann-Whitney test. The effects of OTUD6B-AS1 on thyroid carcinoma cells were determined via the MTT and transwell assays. The potential targets of OTUD6B-AS1 were screened using the online programs OncomiR and StarBase 3.0, and the LncBase Predicted v.2. Luciferase reporter assay was used to confirm the interactions between OTUD6B-AS1 and its potential targets.Results: OTUD6B-AS1 was downregulated in thyroid carcinoma tissue samples. The expression of OTUD6B-AS1 correlated with tumor size, clinical stage, and lymphatic metastasis of thyroid carcinoma. Overexpression of OTUD6B-AS1 significantly decreased the viability, migration, and invasion of thyroid carcinoma cells. Online programs predicted miR-183-5p and miR-21 as potential targets of OTUD6B-AS1. Luciferase reporter assays showed miR-183-5p and miR-21 bound to OTUD6B-AS1. Moreover, overexpression of miR-183-5p and miR-21 compromised the inhibitory effects of OTUD6B-AS1 on viability, migration, and invasion of thyroid carcinoma cells.Conclusions: Taken together, our findings present in vitro evidence of lncRNA OTUD6B-AS1 as a tumor suppressor in thyroid carcinomas. OTUD6B-AS1 inhibits viability, migration, and invasion of thyroid carcinoma by targeting miR-183-5p and miR-21.

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“…Determination of cell viability by MTT assay. Cell viability was examined by MTT assay following previously described methods (25). The Od values were measured at 490 nm using microplate reader (Bio-Rad Laboratories, Inc.).…”

Section: Cell Lines and Cell Transfectionmentioning

confidence: 99%

“…Western blot analysis. The protein levels of α-smooth muscle actin (α-SMA), collagen I and Napsin A were examined by western blot analysis following previously described methods (25). A total of 50 µg protein samples were then separated by 10% SDS-PAGE and transferred onto nitrocellulose membrane (Bio-Rad Laboratories, Inc.).…”

Section: Cell Lines and Cell Transfectionmentioning

confidence: 99%

TGF‑β1 induces CREB1‑mediated miR‑1290 upregulation to antagonize lung fibrosis via Napsin�A

Guan

Zhang

et al. 2020

Int J Mol Med

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The pathologic mechanisms of pulmonary fibrosis (PF), one of the most common chronic pulmonary diseases, remain unclear. Napsin A is an aspartic proteinase that has been regarded as a hallmark of pulmonary adenocarcinoma. The present study aimed to investigate the specific function and molecular mechanisms of Napsin A in PF from the perspective of microRNA (miRNA or miR) regulation. In the present study, it was found that miR-1290 downregulated the expression of Napsin A by binding to its 3'-UTR. Cell viability was examined by MTT assay. The protein levels of α-smooth muscle actin (α-SMA), Collagen I and Napsin A were examined by western blot analysis. The predicted targeting of Napsin A by miR-1290 was validated by luciferase reporter assay. The protein content of α-SMA was examined by immunofluorescence staining. miR-1290 was found to be upregulated in blood samples from patients with PF and in TGF-β1-stimulated A549 cells. miR-1290 was found to directly target Napsin A. miR-1290 overexpression also significantly promoted A549 cell proliferation and increased the protein levels of markers of fibrosis. Napsin A knockdown exerted effects on A549 cell proliferation and TGF-β1-induced fibrosis that were similar to those induced by miR-1290 overexpression; more importantly, Napsin A knockdown significantly reversed the effects of miR-1290 inhibition, indicating that miR-1290 promotes TGF-β1-induced fibrosis by targeting Napsin A. Moreover, TGF-β1-induced CAMP responsive element binding protein 1 (cREB1) overexpression promoted the transcription of miR-1290 in A549 cells. On the whole, the findings of the present study demonstrate that TGF-β1-induced cREB1 overexpression induces the significant upregulation of miR-1290 expression, thus aggravating TGF-β1-induced fibrotic changes in A549 cells via the miR-1290 downstream target, Napsin A.

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LncRNA XIST/miR-34a axis modulates the cell proliferation and tumor growth of thyroid cancer through MET-PI3K-AKT signaling

Cited by 251 publications

References 41 publications

Ozone therapy promotes the differentiation of basal keratinocytes via increasing Tp63‐mediated transcription of KRT10 to improve psoriasis

Ozone therapy promotes the differentiation of basal keratinocytes via increasing Tp63‐mediated transcription of KRT10 to improve psoriasis

OTUD6B-AS1 Inhibits Viability, Migration, and Invasion of Thyroid Carcinoma by Targeting miR-183-5p and miR-21

TGF‑β1 induces CREB1‑mediated miR‑1290 upregulation to antagonize lung fibrosis via Napsin�A

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