Elastic Silicone Occlusive Sheeting Versus Silicone Occlusive Sheeting in the Treatment of Scars: A Randomized Controlled Trial.

INTRODUCTION: Hypertrophic scarring caused by conventional open thyroidectomy is prevalent among Asians and published trials have proved that silicone occlusive sheeting is a useful treatment for hypertrophic scarring. However, silicone occlusive sheeting does not effectively prevent scar widening. Here, we report elastic silicone occlusive sheeting as a new type of silicone application. In this study, we compared the effects of elastic silicone occlusive sheeting on scar width and appearance after conventional open thyroidectomy with those of silicone occlusive sheeting. METHODS: In this prospective, randomized, assessor-blinded study, a total of 74 patients who underwent conventional open thyroidectomy were recruited to undergo elastic silicone occlusive sheeting and silicone occlusive sheeting on the healed wound. Split scar study and scar quality were assessed on the basis of scar width, Vancouver scar scale, pain/itching visual analogue scale, and patients' subjective degree of satisfaction with the scar, during the patients' 6-month review. RESULTS: A total of 61 patients completed the study. Scar width, Vancouver scar scale score, and patients' subjective degree of satisfaction indicated that elastic silicone occlusive sheeting was associated with narrower scars and significant improvement in scar appearance. The two methods did not differ significantly with regard to pain/itching visual analogue scale. CONCLUSIONS: Our findings highlight elastic silicone occlusive sheeting as an effective treatment for scarring, resulting in narrower and better scars after conventional open thyroidectomy. The use of elastic silicone occlusive sheeting after conventional open thyroidectomy may minimize the formation of hypertrophic scars in the early postoperative period. TRIAL REGISTRATION: ChiCTR2100049740.

Long noncoding RNA RP11-757G1.5 sponges miR-139-5p and upregulates YAP1 thereby promoting the proliferation and liver, spleen metastasis of colorectal cancer.

BACKGROUND: Accumulating evidence indicates that long non-coding RNAs (lncRNAs) acting as crucial regulators in tumorigenesis. However, its biological functions of lncRNAs in colorectal cancer (CRC) have not been systematically clarified. METHODS: An unbiased screening was performed to identify disregulated lncRNAs revealed to be implicated in CRC carcinogenesis according to an online-available data dataset. In situ hybridization (ISH), RT-qPCR and RNA fluorescence in situ hybridization (RNA-FISH) were applied to detect RP11-757G1.5 expression in CRC tissues and cell lines. The associations of RP11-757G1.5 with clinicopathological characteristics were analyzed. Their effects on prognosis were analyzed by the Kaplan-Meier analysis, Log-rank test, Univariate and Multivariate Cox regression analysis. The potential biological function of RP11-757G1.5 in CRC was investigated by Colony formation, Edu cell proliferation, Flow cytometry, Wound healing and Transwell assays. Bioinformatics binding site analysis, Luciferase reporter assay, Ago2 immunoprecipitation assays, RNA pull-down assay, RT-qPCR and Western blotting were utilized to demonstrate the mechanism of RP11-757G1.5 acts as a molecular sponge of miR-139-5p to regulate the expression of YAP1. Finally, we further explore the potential role of RP11-757G1.5 in CRC orthotopic xenografts in vivo. RESULTS: We discovered a novel oncogenic lncRNA RP11-757G1.5, that was overexpressed in CRC tissues, especially in aggressive cases. Moreover, up-regulation of RP11-757G1.5 strongly correlated with poor clinical outcomes of patients with CRC. Functional analyses revealed that RP11-757G1.5 promoted cell proliferation in vitro and in vivo. Furthermore, RP11-757G1.5 stimulated cell migration and invasion in vitro and in vivo. Mechanistic studies illustrated that RP11-757G1.5 regulated the expression of YAP1 through sponging miR-139-5p and inhibiting its activity thereby promoting CRC progression and development. CONCLUSIONS: Altogether, these results reveal a novel RP11-757G1.5/miR-139-5p/YAP1 regulatory axis that participates in CRC carcinogenesis and progression.

RBFOX3 Promotes Gastric Cancer Growth and Progression by Activating HTERT Signaling.

Tumor invasion, metastasis, and recrudescence remain a considerable challenge in the treatment of gastric cancer (GC). Herein we first identified that RNA binding protein fox-1 homolog 3 (RBFOX3) was markedly overexpressed in GC tissues and negatively linked to the survival rate of GC patients. RBFOX3 promoted cell division and cell cycle progression in vitro and in vivo. Furthermore, RBFOX3 increased the cell invasion and migration ability. The suppression of GC cell multiplication and invasion, caused by silencing of RBFOX3, was rescued by HTERT overexpression. Additionally, RBFOX3 augmented the resistance of GC cells to 5-fluorouracil by repressing RBFOX3. Mechanistically, the exogenous up-regulation of RBFOX3 triggered promoter activity and HTERT expression, thereby enhancing the division and the development of GC cells. Further co-immunoprecipitation tests revealed that RBFOX3 bound to AP-2ß to modulate HTERT expression. In conclusion, our study indicates that a high expression of RBFOX3 promotes GC progression and development and predicts worse prognosis. Collectively, these results indicate that the RBFOX3/AP-2ß/HTERT signaling pathway can be therapeutically targeted to prevent and treat GC recurrence and metastasis.