&lt;p&gt;miR-27b Suppresses Tongue Squamous Cell Carcinoma Epithelial–Mesenchymal Transition by Targeting ITGA5&lt;/p&gt;

Li, Tao; Wu, Qian; Liu, Duanqin; Wang, Xuxia

doi:10.2147/ott.s281211

Cited by 17 publications

(14 citation statements)

References 29 publications

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“…miR-27b has been reported to be a tumor suppressor gene. miR-27b can inhibit epithelial-mesenchymal transition andinhibit the proliferation and migration of oral squamous cell carcinoma by targeting integrin subunit α5( 11 ). In addition, miR-27b inhibited the growth and metastatic behavior of ovarian cancer cells by targeting C-X-C motif chemokine ligand 1( 12 ).…”

Section: Resultsmentioning

confidence: 99%

LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b

et al. 2021

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The association between long intergenic non-protein-coding RNA 963 (LINC00963) and diabetes has not been fully elucidated. Therefore, the present study aimed to investigate the effect of the long non-coding RNA LINC00963 on diabetic retinopathy (DR), in order to provide a new therapeutic target for this condition. Human retinal capillary endothelial cells (HRECs) were induced with high concentrations of glucose to establish a DR model. The expression levels of LINC00963, cell viability, the protein expression levels of proliferating cell nuclear antigen (PCNA) and Ki67, and the migratory capacity of HRECs were determined using reverse transcription-quantitative PCR (RT-qPCR), Cell Counting Kit-8 assay, western blot analysis, and wound healing and Transwell assays, respectively. Furthermore, the Encyclopedia of RNA Interactomes database was used to predict the binding targets of LINC00963, and luciferase reporter assay was used to verify the direct binding of microRNA (miR)-27b to LINC00963. RT-qPCR was also utilized to measure the expression levels of miR-27b, PCNA and Ki67. The results demonstrated that LINC00963 silencing inhibited glucose-induced HREC proliferation and migration, and downregulated PCNA and Ki67 expression. Following transfection with miR-27b inhibitor, cell proliferation and migration were notably enhanced, and the protein expression levels of PCNA and Ki67 were increased. Taken together, the results of the present study suggested that the LINC00963/miR-27b axis may regulate the proliferation and migration of glucose-induced HRECs. Therefore, LINC00963 may be considered as a potential therapeutic target for DR.

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Section: Resultsmentioning

confidence: 99%

LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b

et al. 2021

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“…The experimental methods and reagents were introduced in our previous studies. 20 The primary antibodies used in this study were as follows, cyclin A2 (ab181591), c-Myc (ab32072), E2F2 (ab138515) and GAPDH (ab181602). The bands were finally analyzed by the ImageJ software.…”

Section: Methodsmentioning

confidence: 99%

Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

Li¹,

Liu²,

Li³

et al. 2021

CMAR

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Background: Evidence has indicated that dysregulation of long noncoding RNAs (lncRNA) is a critical factor in the occurrence of many diseases, including cancer. The lncRNA AFAP1-AS1 has been shown to participate in oncogenesis, metastasis, or drug resistance in many types of cancer. However, the potential role of AFAP1-AS1 in oral squamous cell carcinoma (OSCC) has not been fully elucidated. Methods: Bioinformatics analysis was performed to compare AFAP1-AS1 expression levels in OSCC cancer samples and in normal controls. The biological function of AFAP1-AS1 was studied through loss-of-function assays. To study the potential mechanisms, high-throughput sequencing was applied to OSCC cancer samples and a series of bioinformatics analyses were performed. The effects of AFAP1-AS1 on OSCC tumor growth was evaluated by in vivo xenograft tumor formation assays. Results: Bioinformatics analyses indicated that AFAP1-AS1 was upregulated in OSCC. Overexpression of AFAP1-AS1 was positively correlated with lymph node metastasis, tumor stage, and pathological grade. Down-regulation of AFAP1-AS1 in OSCC led to decreased proliferation in vitro and, notably, inhibition of tumor growth in vivo. Further research indicated that AFAP1-AS1 regulated OSCC cell proliferation by targeting CCNA2. Conclusion: AFAP1-AS1 promotes tumor proliferation and indicates a poor prognosis in OSCC, providing a potential therapeutic strategy.

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“…Micro-RNAs (miRNAs) are not only important regulators of cell proliferation, differentiation, and apoptosis but also closely related to cell phenotype and human diseases [15]. Emerging evidence has indicated that upregulated miR-27b-5p (miR-27b) and miR-92a-1-3p (miR-92a) levels contribute to various types of cancers [16][17][18][19]. e overexpression of miR-92a has been shown to promote cellular activity and suppress the sensitivity of lung cancer cells to gefitinib [20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Mangiferin Inhibits Human Lung Adenocarcinoma by Suppressing MiR-27b and MiR-92a

Chi

Meng

Chen

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Lung adenocarcinoma (LUAD) is one of the most prevalent malignancies. However, its mechanism and therapeutic strategy remain to be clarified. Mangiferin is a flavonoid derived from the leaves of mango trees of the lacquer family that has many pharmacological and physiological effects. This research aimed to elucidate the biological effect of mangiferin in LUAD cell lines and clarify the in vitro mechanism of mangiferin. Mangiferin was shown to significantly restrain the proliferation of LUAD cells (A549, H1299, and H2030 cells) in a dose- and time-dependent manner. Furthermore, mangiferin was capable of stimulating apoptosis, and more cells were blocked in G1 and S phase in the mangiferin-treated cells than in those not treated with mangiferin. Microarrays and micro-RNA sequencing data suggested that there is a higher level of miR-27b and miR-92a in LUAD tissues than in non-LUAD tissues. Additional experiments indicated that mangiferin may be related to the downregulated levels of miR-92a and miR-27b. In conclusion, mangiferin likely regulates proliferation and apoptosis in LUAD cells by reducing the expression levels of miR-92a and miR-27b.

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<p>miR-27b Suppresses Tongue Squamous Cell Carcinoma Epithelial–Mesenchymal Transition by Targeting ITGA5</p>

Cited by 17 publications

References 29 publications

LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b

LINC00963 silencing inhibits the proliferation and migration of high glucose‑induced retinal endothelial cells via targeting miR‑27b

Silencing of LncRNA AFAP1-AS1 Inhibits Cell Proliferation in Oral Squamous Cancer by Suppressing CCNA2

Mangiferin Inhibits Human Lung Adenocarcinoma by Suppressing MiR-27b and MiR-92a

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