Increasing researches have focused on the biological functions of long noncoding RNAs (lncRNAs) in human cancers. HOXA11-AS, a widely known lncRNA, has been confirmed to be involved in the progression of several cancers, including gastric cancer (GC). Whereas, the detailed mechanism of this lncRNA in GC remains to be further illuminated. The abundances of HOXA11-AS, miR-148a and WNT1 in GC tissues and cell lines were examined by qRT-PCR. Clinicopathological and Kaplan-Meier survival analyses were determined to explore the relationship between HOXA11-AS expression and outcomes of patients. Transwell assay was performed for the evaluation of cell migration and invasion. Bioinformatics, dual-luciferase reporter and RNA immunoprecipitation assays were employed to analyze the correlation between HOXA11-AS and miR-148a or miR-148a and WNT1. The protein levels of WNT1 and β-catenin were assessed by western blot assay. Results showed that HOXA11-AS and WNT1 expression levels were upregulated, while miR-148a level was downregulated in GC tissues and cell lines relative to matched controls. Elevated expression of HOXA11-AS was associated with increased tumor size, lymph node metastasis, advanced TNM stage, as well as reduced survival of GC patients. HOXA11-AS induced migration and invasion of GC cells through serving as a molecular sponge for miR-148a. Furthermore, miR-148a inactivated WNT1/β-catenin signaling pathway via directly targeting WNT1. HOXA11-AS increased WNT1/β-catenin pathway activity, which was abolished by miR-148a overexpression in GC cells. In conclusion, overexpression of HOXA11-AS contributed to migration and invasion of GC cells via activation of WNT1/β-catenin signaling pathway through repressing miR-148a, providing a prospective therapeutic target for GC.

Objective: Retinoblastoma (RB) is a frequent eye cancer in children. Long non-coding RNA (LncRNA) HOXA transcript at the distal tip (HOTTIP) is aberrantly expressed in cancer tissues. This study explores the underlying mechanism of lncRNA HOTTIP in RB. Methods: HOTTIP expression in normal retinal cells and RB cell lines was detected using qRT-PCR. The proliferation of RB cells was measured using CCK-8 and EdU assays, and apoptosis was detected using flow cytometry and Western blotting after the transfection of si-HOTTIP into Y79 cells and pc-HOTTIP into HXO-RB-44 cells. The target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1 were predicted by bioinformatics website and verified using dual-luciferase reporter gene assay. The binding of HOTTIP and miR-101-3p was verified using RNA pull-down assay. STC1 mRNA and protein in RB cells were measured using qRT-PCR and Western blotting. Moreover, si-HOTTIP and in-miR-101-3p/in-NC, and si-HOTTIP and pc-STC1/pcDNA were co-transfected into Y79 cells respectively to evaluate cell proliferation and apoptosis. Xenograft study was conducted, and Ki67-positive expression was detected using immunohistochemical staining. Results: HOTTIP expression was promoted in RB tissues and cells. Downregulation of HOTTIP inhibited proliferation and promoted apoptosis of Y79 cells, while upregulation of HOTTIP promoted proliferation and inhibited apoptosis of HXO-RB-44 cells. There were target relationships between HOTTIP and miR-101-3p, and miR-101-3p and STC1. Inhibition of miR-101-3p or overexpression of STC1 reversed the effect of si-HOTTIP on the proliferation and apoptosis of RB cells. Xenograft study showed that knockdown of HOTTIP suppressed the growth of RB in vitro. Conclusion: It could be concluded that HOTTIP sponged miR-101-3p to upregulate STC1 expression, thereby promoting RB cell proliferation and inhibiting apoptosis.

Glaucoma is caused by excessive aqueous humor in the eye, resulting in a continuous or intermittent increase of intraocular pressure, which exceeds the tolerance of the eyeball and damages the optic nerve. Existing treatments for glaucoma do not work well or have significant side effects. Intraocular pressure signal is a very important physiological signal that needs real-time and accurate monitoring in glaucoma patients, especially in severe glaucoma patients. Therefore, long-term, real-time, and accurate monitoring of intraocular pressure is of great significance for the diagnosis and treatment of glaucoma patients. The use of wearable devices for real-time ocular diagnosis and treatment of glaucoma patients is an effective approach. However, the current commonly used intraocular pressure measurement and monitoring technology is difficult to meet the diagnosis and monitoring needs of glaucoma patients in terms of size, measurement accuracy, power consumption, and intelligence. Therefore, facing the needs of glaucoma disease treatment, this topic studies an implantable flexible intraocular pressure sensor for long-term continuous monitoring of intraocular pressure in glaucoma patients and mainly focuses on the working principle, structural design, process fabrication, measurement and control system, characterization, and performance test of the intraocular pressure sensor. It is of great significance for personalized and accurate treatment of glaucoma patients.