FOXM1 (forkhead box protein M1) is a critical proliferation-associated transcription factor that is widely spatiotemporally expressed during the cell cycle It is closely involved with the processes of cell proliferation, self-renewal, and tumorigenesis In most human cancers, FOXM1 is overexpressed, and this indicates a poor prognosis for cancer patients FOXM1 maintains cancer hallmarks by regulating the expression of target genes at the transcriptional level Due to its potential role as molecular target in cancer therapy, FOXM1 was named the Molecule of the Year in 2010 However, the mechanism of FOXM1 dysregulation remains indistinct A comprehensive understanding of FOXM1 regulation will provide novel insight for cancer and other diseases in which FOXM1 plays a major role Here, we summarize the transcriptional regulation, post-transcriptional regulation and post-translational modifications of FOXM1, which will provide extremely important implications for novel strategies targeting FOXM1

/pdf/regulation-of-the-master-regulator-foxm1-in-cancer-3vbnu6loo4.pdf

Regulation of the master regulator FOXM1 in cancer

Diagnostic, prognostic, and therapeutic significance of long non-coding RNA MALAT1 in cancer.

A Systematic Review of miR-29 in Cancer.

Cellular stress response is a universal mechanism that ensures the survival or negative selection of cells in challenging conditions. The transcription factor Forkhead box protein O3 (FOXO3a) is a core regulator of cellular homeostasis, stress response, and longevity since it can modulate a variety of stress responses upon nutrient shortage, oxidative stress, hypoxia, heat shock, and DNA damage. FOXO3a activity is regulated by post-translational modifications that drive its shuttling between different cellular compartments, thereby determining its inactivation (cytoplasm) or activation (nucleus and mitochondria). Depending on the stress stimulus and subcellular context, activated FOXO3a can induce specific sets of nuclear genes, including cell cycle inhibitors, pro-apoptotic genes, reactive oxygen species (ROS) scavengers, autophagy effectors, gluconeogenic enzymes, and others. On the other hand, upon glucose restriction, 5′-AMP-activated protein kinase (AMPK) and mitogen activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) -dependent FOXO3a mitochondrial translocation allows the transcription of oxidative phosphorylation (OXPHOS) genes, restoring cellular ATP levels, while in cancer cells, mitochondrial FOXO3a mediates survival upon genotoxic stress induced by chemotherapy. Interestingly, these target genes and their related pathways are diverse and sometimes antagonistic, suggesting that FOXO3a is an adaptable player in the dynamic homeostasis of normal and stressed cells. In this review, we describe the multiple roles of FOXO3a in cellular stress response, with a focus on both its nuclear and mitochondrial functions.

FOXO3a from the Nucleus to the Mitochondria: A Round Trip in Cellular Stress Response.

https://link.springer.com/content/pdf/10.1007%2Fs13311-018-0649-9.pdf

LncRNA PVT1 Facilitates Tumorigenesis and Progression of Glioma via Regulation of MiR-128-3p/GREM1 Axis and BMP Signaling Pathway

Background As a novel inflammatory marker, Systemic Immune-Inflammation Index (SII) has not been studied with hepatic steatosis. The aim of this study was to investigate the possible relationship between SII and hepatic steatosis. Methods In the cross-sectional investigation, adults having complete information on SII, hepatic steatosis, and bariatric surgery from the 2015–2018 National Health and Nutrition Examination Survey (NHANES) were included. Hepatic steatosis was evaluated with heaptic steatosis index (HSI). The platelet count × neutrophil count/lymphocyte count was used to compute SII. We investigated the independent interaction between SII and hepatic steatosis using weighted multivariable regression analysis and subgroup analysis. To explore the potential relationship between SII, bariatric surgery and hepatic steatosis by controlling potential confounders by propensity score matching. Results The study involved 10505 participants in total, 5937 (56.5%) of whom had hepatic steatosis according to the diagnosis. After adjusted for covariates, multivariable logistic regression revealed that high SII level was an independent risk factor for hepatic steatosis (OR = 1.30, 95% CI: 1.10-1.52, P 0.01). Unexpectedly, bariatric surgery reduced SII even after PSM corrected for differences of BMI and HSI. Conclusions In US adults, SII was positively correlated with an increase in hepatic steatosis. The SII may be a simple and affordable way to identify hepatic steatosis. Bariatric surgery may reduce SII without resorting to weight loss. This needs to be verified in additional prospective research.

/pdf/systemic-immune-inflammation-index-is-associated-with-2o1dhk99.pdf

Systemic immune-inflammation index is associated with hepatic steatosis: Evidence from NHANES 2015-2018

Chrysin ameliorates cerebral ischemia/reperfusion (I/R) injury in rats by regulating the PI3K/Akt/mTOR pathway

Neural stem cells (NSCs) play major roles in neurological recovery after cerebral infarction (CI). This study was trying to investigate whether miR-200a, a vital regulator in cell proliferation, migration and apoptosis, also has a role in oxygen-glucose deprivation/reperfusion (OGD/R) injured NSCs. In this study, primary NSCs were subjected to OGD/R conditions to mimic an in vitro CI model. Before OGD/R induction, NSCs were transfected with vector or shRNA against miR-200a to overexpress or suppress miR-200a expression. The changes in cell viability, apoptosis, migration, the expression of c-Myc, and the phosphorylation of STAT1, STAT3 and MAPK were respectively assessed. Inhibitors of STAT1/3 and MAPK, i.e., Nifuroxazide and BIRB 796, were used to administrate miR-200a-silenced NSCs, and the expressions of above mentioned proteins were detected. After OGD/R exposure, miR-200a was up-regulated in NSCs (P < 0.001). miR-200a silencing alleviated OGD/R-induced the decrease of cell viability and migration (P < 0.01); meanwhile, alleviated OGD/R-induced apoptosis via reducing Bax/Bcl-2 ratio and down-regulating p53 and cytochrome c (P < 0.01 or P < 0.001). c-Myc, p-STAT1, p-STAT3, p-MAPK were all negatively regulated by miR-200a (P < 0.01 or P < 0.001); more important, the increase of c-Myc induced by miR-200a silencing was abolished by Nifuroxazide or BIRB 796 (P < 0.01 or P < 0.001). These data indicate miR-200a silencing protects NSCs from OGD/R-induced injury, possibly via regulating the STATs/c-Myc and MAPK/c-Myc signalings.

/pdf/microrna-200a-silencing-protects-neural-stem-cells-against-41iospzxa6.pdf

microRNA-200a silencing protects neural stem cells against cerebral ischemia/reperfusion injury

Background and Purpose: This study aimed to investigate the efficacy and safety of balloon dilatation and thrombus extraction for the treatment of cerebral venous sinus thrombosis (CVST). Materials and Methods: Twenty-six cases of digital subtraction angiography-confirmed CVST were treated with balloon dilatation and thrombus extraction. Active treatment of primary disease was carried out after cerebral venous sinus recanalization, and the subsequent anticoagulant therapy lasted for 6 months. Results: Recanalization of the cerebral venous sinus was achieved in all 26 patients, and no endovascular treatment-related complications occurred during or after the procedure. At discharge, the Glasgow Coma Scale (GCS) of the patients had improved from an average of 12.3 points to 15 points, and clinical symptoms were improved in 100% of the patients. Follow-up times ranged from 12-62 months (mean follow-up time of 42.3 months) and no thrombus re-formation or new neurological deficits occurred during that time. Conclusion: Based on our small study population, balloon dilatation and thrombus extraction appears to be a safe and effective treatment for cerebral venous sinus thrombosis. However, further research is needed to confirm this.

Balloon dilatation and thrombus extraction for the treatment of cerebral venous sinus thrombosis

MicroRNA-320 Enhances Radiosensitivity of Glioma Through Down-Regulation of Sirtuin Type 1 by Directly Targeting Forkhead Box Protein M1.

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