Pyroptosis is a type of proinflammatory programmed cell death mediated by caspase 1 activity and occurs in several types of eukaryotic tumor cells, including gliomas. MicroRNAs (miRNAs), small endogenous noncoding RNAs, have been demonstrated to be advantageous in glioma therapy. However, the question of whether miRNAs regulate pyroptosis in glioma remains unknown. The current study found that caspase 1 expression was substantially increased in both glioma tissues and glioma cell lines, U87 and T98G, while miR-214 expression was significantly downregulated. Luciferase reporter assay recognized caspase 1 as a target gene of miR-214. These findings demonstrate that miR-214 could inhibit cell proliferation and migration through the regulation of pyroptosis intermediated by caspase 1 in glioma U87 and T98G cells and may suggest a novel therapeutic for the intervention of glioma.

Glioma is a common type of malignant brain tumor characterized by aggressive metastasis capability. Recent evidence has suggested that noncoding RNAs, including microRNAs, have important functions in the pathophysiology of glioma development. In this study, we investigated the biological function of miR-422a in human glioma. We found that miR-422a was downregulated in glioma tissues. We also demonstrated that expression of miR-422a in glioma cells markedly suppressed cell proliferation, migration, and invasion. In addition, we identified insulin-like growth factor 1 (IGF1) and IGF1 receptor (IGF1R) as inhibitory targets of miR-422a in glioma cells. We established that the expression levels of miR-422a were negatively correlated with the expression levels of IGF1/IGF1R and the clinical parameters in glioma patients. An IGFR inhibitor, AG1024, completely blocked the activity of miR-442a on glioma cell proliferation and invasion, which further confirmed that miR-422a functions through IGF1 and IGF1R.

Glioblastoma multiform is one of the most common and most aggressive brain tumors in humans. The molecular and cellular mechanisms responsible for the onset and progression of GBM are elusive and controversial. The function of tumor suppressor candidate 3 (TUSC3) has not been previously characterized in GBM. TUSC3 was originally identified as part of an enzyme complex involved in N-glycosylation of proteins, but was recently implicated as a potential tumor suppressor gene in a variety of cancer types. In this study, we demonstrated that the expression levels of TUSC3 were downregulated in both GBM tissues and cells, and also found that overexpression of TUSC3 inhibits GBM cell proliferation and invasion. In addition, the effects of increased levels of methylation on the TUSC3 promoter were responsible for decreased expression of TUSC3 in GBM. Finally, we determined that TUSC3 regulates proliferation and invasion of GBM cells by inhibiting the activity of the Akt signaling pathway.

Early research on the impact of COVID-19 on academic scientists suggests that disruptions to research, teaching, and daily work life are not experienced equally. However, this work has overwhelmingly focused on experiences of women and parents, with limited attention to the disproportionate impact on academic work by race, disability status, sexual identity, first-generation status, and academic career stage. Using a stratified random survey sample of early-career academics in four science disciplines (N = 3,277), we investigated socio-demographic and career stage differences in the effect of the COVID-19 pandemic along seven work outcomes: changes in four work areas (research progress, workload, concern about career advancement, support from mentors) and work disruptions due to three COVID-19 related life challenges (physical health, mental health, and caretaking). Our analyses examined patterns across career stages as well as separately for doctoral students and for postdocs/assistant professors. Overall, our results indicate that scientists from marginalized (i.e., devalued) and minoritized (i.e., underrepresented) groups across early career stages reported more negative work outcomes as a result of COVID-19. However, there were notable patterns of differences depending on the socio-demographic identities examined. Those with a physical or mental disability were negatively impacted on all seven work outcomes. Women, primary caregivers, underrepresented racial minorities, sexual minorities, and first-generation scholars reported more negative experiences across several outcomes such as increased disruptions due to physical health symptoms and additional caretaking compared to more privileged counterparts. Doctoral students reported more work disruptions from life challenges than other early-career scholars, especially those related to health problems, while assistant professors reported more negative changes in areas such as decreased research progress and increased workload. These findings suggest that the COVID-19 pandemic has disproportionately harmed work outcomes for minoritized and marginalized early-career scholars. Institutional interventions are required to address these inequalities in an effort to retain diverse cohorts in academic science.

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