Lufei Wang

In recent years, macular foveoschisis has emerged as a prevalent complication in individuals with high myopia, primarily resulting from the synergistic effect of inward traction by vitreoretinal adhesions and outward traction exerted by posterior scleral staphyloma on the retina. While some maintain partial visual stability over an extended period, others may progress to macular holes or even retinal detachment. The primary surgical interventions include vitrectomy, macular buckling, and posterior scleral reinforcement. However, the application of inner limiting membrane peeling and gas tamponade remains a subject of ongoing debate concerning their necessity and efficacy. This review comprehensively addresses the classification, pathogenesis, natural progression, concomitant pathologies, and therapeutic strategies for macular foveoschisis in highly myopic patients.

Background: As a common ocular complication of diabetes mellitus, diabetic cataract is becoming a leading cause of visual impairment. The progression of diabetic cataract progression involves epithelial-to-mesenchymal transition (EMT), the precise role of which remains to be investigated. As microRNAs (miRNAs) are suggested to be involved in the pathogenesis of many diseases, identification of aberrantly expressed miRNAs in diabetic lens epithelial cells (LECs) and their targets may provide insights into our understanding of diabetic cataract and potential therapeutic targets. Methods: Diabetic cataract capsules and LECs exposed to high glucose (25 mmol/L, 1–5 days) were used to mimic the model. Quantitative RT-PCR was performed to evaluate the differential expression of miRNA. Dual luciferase reporter assay was used to identify the binding target of miR-199a-5p. The expression of EMT-associated proteins was determined by immunofluorescence and Western blot analysis. Results: Our results showed the differential expression of miR-9, -16, -22, -199a and -204. MiR-199a was downregulated in diabetic cataract capsule and hyperglycemia-conditioned human LECs. Specific protein 1 could be directly targeted and regulated by miR-199a in LECs and inhibit EMT in diabetic LECs. Conclusion: Our findings implied miR-199a could be a therapeutic target by regulating SP1 directly to affect EMT in diabetic cataract and provided novel insights into the pathogenesis of diabetic cataract.

Dioscin is a typical saponin with multiple pharmacological activities. The past few years have seen an emerging interest in and growing research on this pleiotropic saponin. Here, we review the emerging pharmacological activities reported recently, with foci on its antitumor, antimicrobial, anti-inflammatory, antioxidative, and tissue-protective properties. The potential use of dioscin in therapies of diverse clinical disorders is also discussed.

The long noncoding RNA nuclear‐enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. However, the role, expression status, and the detailed mechanism of NEAT1 in retinoblastoma (RB) yet need to be unraveled. We explored the role and the mechanism of NEAT1 activity in RB. Our data show enhanced NEAT1 expression in RB‐affected tissues compared with the corresponding control. Functional experiments reveal that a NEAT1 knockdown in RB cells significantly inhibits proliferation, cycle progression, and facilitates apoptosis and caspase‐3 and ‐9 activities. Besides that, miR‐124 was predicted to be a target of NEAT1 and its reduced expression, as well as the inverse correlation of NEAT1 with miR‐124, was observed in RB‐affected tissues. Further, luciferase and RNA immunoprecipitation (RIP) assays confirmed the interaction between NEAT1 and miR‐124. Rescue experiments confirmed that the inhibition of miR‐124 could reverse the effect of NEAT1 on RB cell proliferation, cycle arrest, apoptosis, and caspase‐3 and ‐9 activities. Thus, NEAT1 promotes RB progression by sponging miR‐124, providing a therapeutic target for RB.

// <![CDATA[ $('.header-date').hide();$('#titleAuthors').hide();$('#abstractHeader').hide(); // ]]> Na Li1, Lufei Wang2, Guangyun Tan3, Zhiheng Guo1, Lei Liu1, Ming Yang4, * and Jin He1, * 1Department of Gynecology and Obstetrics, The First Hospital of Jilin University, Changchun, Jilin 130021, PR China 2Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, Jilin 130022, PR China 3Department of Immunology, Institute of Translational Medicine of The First Hospital of Jilin University, Changchun, Jilin 130021, PR China 4Department of Breast Surgery, The First Hospital of Jilin University, Changchun, Jilin 130021, PR China *These authors have contributed equally to this work Correspondence to: Ming Yang, email: yangming196701@163.com Jin He, email: jinhe1204@126.com Keywords: MiR-218, ovarian cancer, RUNX2, proliferation, invasion Received: April 07, 2017 Accepted: July 19, 2017 Published: September 16, 2017 ABSTRACT MicroRNA-218 (miR-218) has been implicated in the development and progression of multiple cancers. We investigated the role of miR-218 in ovarian cancer progression. We found that miR-218 expression levels were lower in ovarian cancer tissues and cell lines than in adjacent normal tissues or a normal ovarian cell line.miR-218 levels associated with International Federation of Gynecology and Obstetrics (FIGO) stage and lymph node metastasis. Exogenous expression of miR-218 inhibited cell proliferation, colony formation, migration, and invasion in vitro and suppressed tumor growth in a tumor-bearing nude mouse model. Runt-related transcription factor 2 (RUNX2) was identified as a direct functional target of miR-218, and its expression was inversely correlated with miR-218 expression in ovarian cancer tissues. RUNX2 overexpression rescued the suppressive effect of miR-218 on ovarian cancer cell proliferation, colony formation, migration, and invasion. These findings highlight an important role played bymiR-218 in the regulation of cancer growth and metastasis, in part by repressing RUNX2, and revealed the potential of miR-218 as a new therapeutic target inovarian cancer.

A series of recent studies suggested that miR-143 might involve in the tumorigenesis and metastasis of various cancer types. However, the biological function and underlying mechanisms of miR-143 in human epithelial ovarian carcinoma (EOC) remain unknown. Therefore, this study aimed to investigate the miR-143 expression and its clinical diagnosis significance in patients suffering EOC and to analyze its role and underlying molecular mechanism in EOC. Our result showed that the expression levels of miR-143 were downregulated in EOC tissues and cell lines, was associated with International Federation of Gynaecology and Obstetrics (FIGO) stage, pathological grade and lymph node metastasis (all P < 0.01). Overexpression of miR-143 significantly inhibited EOC cell proliferation, migration, and invasion. Furthermore, computational algorithm combined with luciferase reporter assays identified connective tissue growth factor (CTGF) as the direct target of miR-143 in EOC cells. The expression level of CTGF was significantly increased in EOC tissues, was inversely correlated with miR-143 expression in clinical EOC tissues. Knockdown of CTGF mimicked the suppression effect induced by miR-143 overexpression. Restoration of CTGF expression partially reversed the suppression effect induced by miR-143 overexpression. These results suggested that miR-143 inhibited EOC cell proliferation, migration, and invasion, at least in part, via suppressing CTGF expression.

A growing body of evidence suggests that microRNA-494 (miR-494) could act as tumor-suppressive or oncogenic microRNAs (miRNAs) in different types of tumors. However, the biological roles and underlying mechanisms of miR-494 remain unknown in human epithelial ovarian carcinoma (EOC). Therefore, the aims of this study were to investigate the miR-494 expression and the significance of its clinical diagnosis in patients suffering EOC and to analyze its role and underlying molecular mechanism on the carcinogenesis of EOC. Here, we found that miR-494 was significantly decreased in EOC cell lines and tissues and its expression was negatively correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, high pathological grade, and lymph node metastasis (all P < 0.01). Functional studies showed that overexpression of miR-494 in EOC cells could remarkably inhibit proliferation, colony formation, migration, and invasion and induce cell apoptosis, G0/G1 phase arrest. An in vivo analysis revealed that the overexpression of miR-494 suppressed tumor growth in a nude mouse xenograft model system. Bioinformatic assay and dual-luciferase assay confirmed that insulin-like growth factor 1 receptor (IGF1R) was as a direct target of miR-494 in EOC cells. Western blot assay showed that overexpression of miR-494 inhibited IGF1R expression and its downstream signal protein expression. In addition, downregulation of IGF1R has similar effects with miR-494 overexpression on EOC cells and overexpression of IGF1R effectively rescued the inhibition of overexpressed miR-494 in EOC cells. These data suggested that miR-494 functions as a tumor suppressor in EOC by targeting IGF1R.

This is to review the current state of knowledge on the functional and clinical aspects of bestrophin 1, a prominent member of a family of proteins involved in the control and properties of the light peak of the EOG. Initially human bestrophin 1 gene (BEST1) mutations were identified to underlie Best vitelliform macular dystrophy (VMD), a dominantly inherited, juvenile-onset form of macular degeneration. In the recent past the phenotypical spectrum of retinal disorders associated with BEST1 mutations has been extended and the term bestrophinopathies was coined. The physiological role of bestrophin 1 is still not completely understood but has been linked to the generation of a transepithelial chloride current by controlling voltage-dependent calcium channels (VDCC). Dysfunction of bestrophin 1 may result in abnormal ion and fluid transport by the retinal pigment epithelium (RPE) disturbing and even disrupting direct interactions between the RPE and the photoreceptors.