<p>MiRNA-128 and MiRNA-142 Regulate Tumorigenesis and EMT in Oral Squamous Cell Carcinoma Through HOXA10</p>

Abstract

Background: Oral squamous cell carcinoma (OSCC) accounts for more than 90% of all oral cavity cancers, and the 5-year survival rate for OSCC patients remains unsatisfactory. MiRNA-128/miRNA-142 has been reported to work as a tumor suppressor in diverse tumors. However, the biological function of miR-128/miR-142 in OSCC is still unknown. Methods: The expression of miR-128/miR-142 and homeobox A10 (HOXA10) in OSCC tissues and cells was measured by quantitative real-time polymerase chain reaction (RT-qPCR). The effects of miR-128/miR-142 or HOXA10 on proliferation, migration, invasion and apoptosis were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), transwell and flow cytometry assays, respectively. The expression levels of epithelial-mesenchymal transition (EMT)-associated proteins (E-cadherin, N-cadherin and Vimentin), proliferation-associated protein ki-67 and HOXA10 were detected by Western blot assay. The interaction between HOXA10 and miR-128/miR-142 was predicted by TargetScan, and then confirmed by dual-luciferase reporter assay. Results: MiR-128/miR-142 was downregulated in OSCC tissues and cells. Overexpression of miR-128/miR-142 inhibited proliferation, migration, invasion and EMT and induced apoptosis in OSCC cells. HOXA10 as the target of miR-128/miR-142 was verified in OSCC cells. Knockdown of HOXA10 also repressed proliferation, migration, invasion and EMT and boosted apoptosis in OSCC cells. Upregulation of miR-128/miR-142 hindered the expression level of HOXA10, while introduction of HOXA10 weakened the effect. Conclusion: MiR-128/miR-142 suppressed OSCC tumorigenesis and metastasis by targeting HOXA10, providing a new promising therapeutic approach for OSCC patient diagnosis and treatment.

miRNA Profiling of Hungarian Regressive Wilms’ Tumor Formalin-Fixed Paraffin-Embedded (FFPE) Samples by Quantitative Real-Time Polymerase Chain Reaction (RT-PCR)

“…miR-128 is known to affect tumorigenesis in a number of cancer types [ 28 ] and has been suggested to play various regulatory roles in the central nervous system [ 29 , 30 ], but no reports are available linking it to the pathogenesis or prognosis of Wilms’ tumor. The overexpression we initially observed in Patient 1 was not reproducible across all samples, with some showing an elevation and others a decrease ( Table 3 ).…”

Knockdown of lncRNA DLEU1 inhibits the tumorigenesis of oral squamous cell carcinoma via regulation of miR‑149‑5p/CDK6 axis

“…For example, it was previously reported that miR-770 could promote the migration and invasion of OSCC cells by regulating the NAD-dependent protein deacetylase sirtuin-7 (Sirt7)/Smad4 pathway ( 17 ). Moreover, miR-128 and miR-142 could regulate the tumorigenesis and epithelial-mesenchymal transition in OSCC through mediation of homeobox protein Hox-A10 ( 18 ). Meanwhile, Luo et al ( 19 ) found that miR-149-5p could regulate cisplatin chemosensitivity, cell growth, and metastasis of OSCC cells by targeting TGFβ2.…”

miR-375-NAT10 Axis Dysfunction Promotes Oral Cancer Development and Mediates Cdk7 Stabilizing and Cell Cycle Progression

“…Different from deregulation of mRNA expression levels, miRNA expression alterations are mostly due to promoter-related changes 1,57,58 . The role of miRNA deregulation in oral cancer have been explored in several studies, therein, presenting compelling evidence for the involvement of miRNAs in angiogenesis, tumor progression, invasion, etc [58][59][60] . However, the regulatory mechanisms behind miRNA expression deregulation at a genome scale remained largely unknown.…”