Anxiety and Depression in Pediatric-Onset Traumatic Spinal Cord Injury: A Systematic Review.

BACKGROUND: Traumatic spinal cord injury (TSCI) is a debilitating neurological condition with significant long-term consequences on the mental health and well-being of affected individuals. We aimed to investigate anxiety and depression in individuals with pediatric-onset TSCI. METHODS: PubMed, Scopus, and Web of Science databases were searched from inception to December 20th, 2022 following the Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines, and studies were included according to the eligibility criteria. RESULTS: A total of 1013 articles were screened, and 18 studies with 4234 individuals were included in the final review. Of these, 1613 individuals (38.1%) had paraplegia, whereas 1658 (39.2%) had tetraplegia. A total of 1831 participants (43.2%) had complete TSCI, whereas 1024 (24.2%) had incomplete TSCI. The most common etiology of TSCI with 1545 people (36.5%) was motor vehicle accidents. The youngest mean age at the time of injury was 5.92 ± 4.92 years, whereas the oldest was 14.6 ± 2.8 years. Patient Health Questionnaire-9 was the most common psychological assessment used in 9 studies (50.0%). Various risk factors, including pain in 4 studies (22.2%), reduced sleep quality, reduced functional independence, illicit drug use, incomplete injury, hospitalization, reduced quality of life, and duration of injury in 2 (11.1%) studies, each, were associated with elevated anxiety and depression. CONCLUSIONS: Different biopsychosocial risk factors contribute to elevated rates of anxiety and depression among individuals with pediatric-onset TSCI. Individuals at risk of developing anxiety and depression should be identified, and targeted support should be provided. Future large-scale studies with long-term follow-up are required to validate and extend these findings.

LncRNA MACC1-AS1/MACC1 enhances the progression of glioma via regulating metabolic plasticity.

This study plans to investigate the effects of long-noncoding RNA MACC1-AS1 on glioma cells and its mechanism at metabolic plasticity angle. The MACC1-AS1 level was identified both in glioma tissues and in cells. Then the effects of MACC1-AS1 abnormal level on cell viability, apoptosis, the expression of apoptosis associated protein, glucose metabolism and redox status were measured in A172 and U251 cells by different methods. Furthermore, the interaction of MACC1-AS1 and MACC1 in glioma cells was investigated and the role of AMPK pathway was specifically examined. Our results demonstrated that MACC1-AS1 level was high in glioma tissues and cells, and MACC1-AS1 overexpression was closely associated with poor prognosis of glioma. Notably, under glucose deprivation, the MACC1-AS1 level was significantly increased, and overexpression of MACC1-AS1 increased cell viability but inhibited apoptosis. Also, MACC1-AS1 overexpression obviously increased the levels of GLUT1, HK2, G6PD, MCT1, ATP, lactate and NAPDH as well as promoted the activities of HK2 and LDHA, while reduced ROS level and the ratio of NADP+/NAPDH. In particular, the effects of proliferation, apoptosis and metabolic plasticity of glioma cells caused by MACC1-AS1 overexpression were achieved by positively regulating MACC1, and MACC1-AS1 promoted MACC1 expression via the AMPK pathway. In conclusions, the MACC1-AS1/MACC1 axis exertes the tumor-promoting effect by regulating glucose metabolism and redox homeostasis in glioma cells by activating the AMPK signals.

LncRNA NNT-AS1 promote glioma cell proliferation and metastases through miR-494-3p/PRMT1 axis.

Long noncoding RNAs (lncRNAs) are key players in cancer progression. However, the function of lncRNA NNT-AS1 on glioma is unclear. In the present study, a total of 73 tumor tissues and matched adjacent non-tumor tissues were collected, and glioma cell lines were cultured in vitro. mRNA expression was tested using RT-qPCR. The protein expression level was determined using the western blot assay, cell proliferation was measured using the CCK-8 and BrdU proliferation assay, and the cell cycle, cell migration and invasion were determined using flow cytometry analysis, the wound healing assay and transwell, respectively. The results showed that lncNNT-AS1 is significantly up-regulated during the early stages of glioma. In particular, high levels of NNT-AS1 are observed in glioma cell lines compared to human astrocyte (HA) cells. Furthermore, the inhibition of lnc-NNT-AS1 by siRNA interfere attenuates the cell viability, proliferation, migration and invasion of glioma cell lines. Mechanistically, the inhibition of NNT-AS1 directly interacted with miRNA-494-3p, and positively regulated the downstream target PRMT1 in vitro. Further study proved that the overexpression of miRNA-494-3p and the inhibition of PRMT1 could attenuate both glioma cell proliferation and metastases. Collectively, our results indicated that the miR-494-3p-PRMT1 axis is involved the tumor-suppressive effects of NNT-AS1 inhibition, which sheds new light on lncRNA-directed diagnostics and the therapeutics of glioma.

WBSCR22 confers cell survival and predicts poor prognosis in glioma.

Human WBSCR22 is involved in cancer proliferation, invasion and metastasis; however, its function in glioma remains unexplored. In our research, we aimed to investigate the role of WBSCR22 in the development of glioma and its possible molecular mechanisms. Using bioinformatic analysis of public datasets, we determined that WBSCR22 overexpression in glioma specimens was correlated with an unfavorable patient prognosis. Our results revealed that WBSCR22 was highly expressed in glioma cell lines. The loss of WBSCR22 inhibited the growth, invasion and migration of glioma cells, while WBSCR22 overexpression produced the opposite effects. Moreover, we found that WBSCR22 downregulation reduced the phosphorylation of Akt and GSK3ß and decreased the levels of ß-catenin and CyclinD1 in glioma cells. The opposite effects were observed when WBSCR22 was overexpressed. Additionally, we verified with a dual-luciferase reporter assay that WBSCR22 was a direct target of miR-146b-5p. Furthermore, overexpression of miR-146b-5p suppressed WBSCR22 mRNA and protein expression. Notably, the restoration of WBSCR22 expression remarkably reversed the effects of miR-146b-5p overexpression on cell survival, apoptosis and the cell cycle in glioma cells. Collectively, our findings revealed a tumor-promoting role for WBSCR22 in glioma cells, thus providing molecular evidence for WBSCR22 as a novel therapeutic target in glioma.