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BACKGROUND: A wide range of studies have demonstrated that microRNA (miR) plays a crucial role in hypertrophic scars development, and type I collagen is closely related to hypertrophic scar fibroblasts. There might be a relationship between miR-2116-3p and occurrence and development of hypertrophic scars. OBJECTIVE: To investigate the expression and role of miR-2116-3p on human hypertrophic scar fibroblasts. METHODS: Hypertrophic scar tissues were collected from six patients from the First Affiliated Hospital of Xinjiang Medical University and normal skin tissues were collected from another six patients after blepharoplasty in the same unit at the same time. The expression of miR-2116-3p and type I collagen was detected by qRT-PCR. Hypertrophic scar tissues were taken and primary cells were cultured to passages 3 to 6. Hypertrophic scar fibroblasts were divided into negative control group, miR-2116-3p mimic group, and miR-2116-3p inhibitor group, and transfected with corresponding sequences. Cell proliferation was detected by cell counting kit-8 and EdU kit. Cell migration was detected by cell scratch assay, and apoptosis was detected by flow cytometry. Expression of type I collagen, type III collagen and α-smooth muscle actin was detected by western blot and qRT-PCR at protein and mRNA levels, respectively. Dual luciferase reporter assay system was used to carry out targeting assays. RESULTS AND CONCLUSION: The mRNA expression of miR-2116-3p and type I collagen in hypertrophic scar tissues was significantly lower than that in normal skin tissues (P < 0.01). After 24, 48, and 72 hours of transfection, the cell viability of the miR-2116-3p mimic group was significantly lower than that of the negative control group (P < 0.05 or P < 0.01), while the cell viability of miR-2116-3p inhibitor group was significantly higher than that of the negative control group (P < 0.05 or P < 0.01). At 48 hours after transfection, the number of EdU positive cells in the miR-2116-3p mimic group was significantly lower than that in the negative control group, while the number of EdU positive cells in the miR-2116-3p inhibitor group was significantly higher than that in the negative control group (P < 0.05). At 24 hours after transfection, the cell scratch area and apoptotic rate of the miR-2116-3p mimic group were significantly higher than those of the negative control group (P < 0.01), and while the cell scratch area and apoptotic rate of the miR-2116-3p inhibitor group werer significantly lower than those of the negative control group (P < 0.01 or P < 0.05). At 24 hours after transfection, the mRMA and protein expression levels of type I collagen, type II collagen and α-smooth muscle actin were significantly decreased in the miR-2116-3p mimic group (P < 0.05 or P < 0.01) and significantly increased in the miR-2116-3p inhibitor group (P < 0.01) compared with the negative control group. Results from the dual luciferase assay showed that miR-2116-3p could bind to type I collagen. To conclude, the expression of miR-2116-3p is down-regulated in human hypertrophic scar. miR-2116-3p may inhibit the proliferation and migration of human hypertrophic scar fibroblasts and promote their apoptosis by targeting the expression of type I collagen. [ABSTRACT FROM AUTHOR]

Abstract Background Glioblastoma (GBM) is malignant, demanding more attention to the improvement of the diagnosis and therapy. LncRNAs have been implicated in the malignancy of GBM cells. Methods HOXA-AS2, miR-2116-3p and SERPINA3 expression levels in GBM tissues and cell lines were detected by qRT-PCR. Western blotting was performed to detect the protein levels of Bax and Bcl-2. Dual-luciferase reporter assay was for detection of relationship among these factors, together with RIP and RNA pull-down. CCK-8, EdU, wound healing and transwell assays were for detection of the role of HOXA-AS2, miR-2116-3p and SERPINA3 in cell viability, proliferation, migration and invasion in GBM, respectively. Results HOXA-AS2 and SERPINA3 showed higher level in GBM tissues and cell lines. Low level of HOXA-AS2 attenuated GBM cell growth in vitro. Moreover, the anti-tumor impact of silenced HOXA-AS2 was restored by miR-2116-3p inhibitor, but its tumor-promotional effect could be reversed by silenced SERPINA3. Conclusion HOXA-AS2 enhanced GBM cell malignancy through sponging miR-2116-3p and releasing SERPINA3, which might shed light on the diagnosis and therapy for GBM in the future.

Abstract Background Hypertrophic scar (HTS) is a fibrotic disorder of skins and may have repercussions on the appearance as well as functions of patients. Recent studies related have shown that competitive endogenous RNA (ceRNA) networks centering around miRNAs may play an influential role in HTS formation. This study aimed to construct and validate a three-miRNA (miR-422a, miR-2116-3p, and miR-3187-3p) ceRNA network, and explore its potential functions. Methods Quantitative real‑time PCR (qRT‑PCR) was used to compare expression levels of miRNAs, lncRNAs, and genes between HTS and normal skin. Target lncRNAs and genes of each miRNA were predicted using starBase as well as TargetScan database to construct a distinct ceRNA network; overlapping target lncRNAs and genes of the three miRNAs were utilized to develop a three-miRNA ceRNA network. For every network, protein–protein interaction (PPI) network analysis was performed to identify its hub genes. For each network and its hub genes, Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted to explore their possible functions. Results MiR-422a, miR-2116-3p, and miR-3187-3p were all downregulated in HTS tissues and fibroblasts. MiR-422a-based ceRNA network consisted of 101 lncRNAs with 133 genes; miR-2116-3p-centered ceRNA network comprised 85 lncRNAs and 978 genes; miR-3187-3p-derived ceRNA network encompassed 84 lncRNAs as well as 1128 genes. The three-miRNA ceRNA network included 2 lncRNAs with 9 genes, where MAPK1, FOSL2, ABI2, KPNA6, CBL, lncRNA-KCNQ1OT1, and lncRNA-EBLN3P were upregulated. According to GO and KEGG analysis, these networks were consistently related to ubiquitination. Three ubiquitination-related genes (CBL, SMURF2, and USP4) were upregulated and negatively correlated with the expression levels of the three miRNAs in HTS tissues. Conclusions This study identified a three-miRNA ceRNA network, which might take part in HTS formation and correlate with ubiquitination.

Background: Hypertrophic scar (HTS) is a fibrotic disorder of skins and may have repercussions on the appearance as well as functions of patients. Recent studies related have shown that competitive endogenous RNA (ceRNA) networks centering around miRNAs may play an influential role in HTS formation. This study aimed to construct and validate a three-miRNA (miR-422a, miR-2116-3p, and miR-3187-3p) ceRNA network, and explore its potential functions.Methods: Quantitative real‑time PCR (qRT‑PCR) was used to compare expression levels of miRNAs, lncRNAs, and genes between HTS and normal skin. Target lncRNAs and genes of each miRNA were predicted using starBase as well as TargetScan database to construct a distinct ceRNA network; overlapping target lncRNAs and genes of the three miRNAs were utilized to develop a three-miRNA ceRNA network. For every network, protein-protein interaction (PPI) network analysis was performed to identify its hub genes. For each network and its hub genes, Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted to explore their possible functions.Results: MiR-422a, miR-2116-3p, and miR-3187-3p were all downregulated in HTS tissues and fibroblasts. MiR-422a-based ceRNA network consisted of 101 lncRNAs with 133 genes; miR-2116-3p-centered ceRNA network comprised 85 lncRNAs and 978 genes; miR-3187-3p-derived ceRNA network encompassed 84 lncRNAs as well as 1128 genes. The three-miRNA ceRNA network included 2 lncRNAs with 9 genes, where MAPK1, FOSL2, ABI2, KPNA6, CBL, lncRNA-KCNQ1OT1, and lncRNA-EBLN3P were upregulated. According to GO and KEGG analysis, these networks were consistently related to ubiquitination. Three ubiquitination-related genes (CBL, SMURF2, and USP4) were upregulated and negatively correlated with the expression levels of the three miRNAs in HTS tissues.Conclusions: This study identified a three-miRNA ceRNA network, which might take part in HTS formation and correlate with ubiquitination. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is one of the most common digestive malignant tumors globally. Focally amplified lncRNA on chromosome 1 (FALEC) is a novel lncRNA that has been reported to be involved in many biological processes during carcinogenesis. However, its role in CRC remains poorly understood. Gene expression at mRNA or protein level was measured by qRT-PCR or western blot, respectively. In vitro experiments including EdU, colony formation, flow cytometry, wound-healing and transwell assays, as well as in vivo xenograft experiment, were utilized to determine the functional role of FALEC in CRC. Relevant mechanical assays were performed to investigate the underlying molecular mechanism. FALEC was aberrantly up-regulated in CRC. FALEC knockdown could impair CRC cell proliferation, migration and invasion, whereas facilitate cell apoptosis. MiR-2116-3p was revealed to be sponged by FALEC. PIWIL1 was identified as the target of miR-2116-3p. Mechanically, FALEC restored the expression of PIWIL1 via absorbing miR-2116-3p. MiR-2116-3p inhibition and PIWIL1 enrichment could counteract the anti-tumor impact induced by silenced FALEC on the oncogenic behaviors of CRC cells. Our study revealed that FALEC promoted CRC progression via restoring the expression of miR-2116-3p-targeted PIWIL1, suggesting the potential application of targeting FALEC in the treatment of CRC. [ABSTRACT FROM AUTHOR]

Background: It is reported that long noncoding RNAs play an important role in human cancers, including breast cancer (BC). However, the effect of long intergenic non-protein coding RNA 1433 (LINC01433) on BC development remains elusive. Materials and Methods: The expression level of LINC01433 in BC cells and a normal breast epithelial cell (MCF-10A) was determined by quantitative real-time polymerase chain reaction (qRT-PCR). A series of functional assays was applied to measure the bio-function of LINC01433 in BC. Bioinformatics analysis and mechanistic assays were utilized to disclose the underlying mechanism involved in the LINC01433-mediated BC cellular process. Results: qRT-PCR revealed that LINC01433 was highly expressed in BC cells. In function, LINC01433 depletion suppressed BC cell proliferation, migration, and epithelial-mesenchymal transition, but induced cell apoptosis. Mechanically, chromatin immunoprecipitation and luciferase reporter assays suggested that LINC01433 was activated by its upstream transcription factor MYC proto-oncogene (MYC). The interaction between LINC01433 and miR-2116-3p was verified in BC. Additionally, MYC was validated as a target gene of miR-2116-3p. Rescue assays demonstrated that LINC01433 promoted BC cellular process via regulating miR-2116-3p/MYC axis. Conclusion: Our findings revealed a novel positive feedback loop (LINC01433/miR-2116-3p/MYC) in BC progression and discovered the novel functional genes in this BC cellular process. [ABSTRACT FROM AUTHOR]