RND1 inhibits epithelial-mesenchymal transition and temozolomide resistance of glioblastoma via AKT/GSK3-β pathway.

GBM is one of the most malignant tumor in central nervous system. The resistance to temozolomide (TMZ) is inevitable in GBM and the characterization of TMZ resistance seriously hinders clinical treatment. It is worthwhile exploring the underlying mechanism of aggressive invasion and TMZ resistance in GBM treatment.

BCAS3 accelerates glioblastoma tumorigenesis by restraining the P53/GADD45α signaling pathway.

As in many other cancers, highly malignant proliferation and disordered cell division play irreplaceable roles in the exceedingly easy recurrence and complex progression of glioblastoma multiforme (GBM); however, mechanistic studies of the numerous regulators involved in this process are still insufficiently thorough. The role of BCAS3 has been studied in other cancers, but its role in GBM is unclear. Here, our goal was to investigate the expression pattern of BCAS3 in GBM and its potential mechanism of action.

Rho family GTPase 1 (RND1), a novel regulator of p53, enhances ferroptosis in glioblastoma.

Background: Ferroptosis is an iron dependent cell death closely associated with p53 signaling pathway and is aberrantly regulated in glioblastoma (GBM), yet the underlying mechanism needs more exploration. Identifying new factors which regulate p53 and ferroptosis in GBM is essential for treatment.

Methods: Glioma cell growth was evaluated by cell viability assays and colony formation assays.

Development and Verification of Glutamatergic Synapse-Associated Prognosis Signature for Lower-Grade Gliomas.

Lower-grade glioma (LGG) is the most common histology identified in gliomas, a heterogeneous tumor that may develop into high-grade malignant glioma that seriously shortens patient survival time. Recent studies reported that glutamatergic synapses might play an essential role in the progress of gliomas. However, the role of glutamatergic synapse-related biomarkers in LGG has not been systemically researched yet.

WAC, a novel GBM tumor suppressor, induces GBM cell apoptosis and promotes autophagy.

WAC is closely related to the occurrence and development of tumors. However, its role in human glioblastoma (GBM) and its potential regulatory mechanisms have not been investigated. This study demonstrated that WAC is downregulated in GBM, and its low expression predicts a poor prognosis.

Notch intracellular domain regulates glioblastoma proliferation through the Notch1 signaling pathway.

Notch intracellular domain (NICD), also known as the activated form of Notch1 is closely associated with cell differentiation and tumor invasion. However, the role of NICD in glioblastoma (GBM) proliferation and the underlying regulatory mechanism remains unclear. The present study aimed to investigate the expression of NICD and Notch1 downstream gene HES5 in human GBM and normal brain samples and to further detect the effect of NICD on human GBM cell proliferation.

Kiaa0101 serves as a prognostic marker and promotes invasion by regulating p38/snail1 pathway in glioma.

Background: Kiaa0101, a regulator of cell proliferation, is overexpressed in many malignant tumors. However, its role in promoting invasion of glioma is poorly understood. Here, we investigated the effects of Kiaa0101 on glioma invasion and elucidated the underlying mechanisms of action.

Genetic deletion of Rnd3 suppresses apoptosis through NF‑κB signaling in the brain.

Rho family GTPase 3 (RND3) is involved in multiple physiological activities involving the Rho kinase‑dependent signaling pathway. The present study revealed a novel role of RND3 in the regulation of apoptosis in the brain. Using immunofluorescence and TUNEL assays, a decreased rate of brain apoptosis was observed in Rnd3‑knockout mice.

RND2 attenuates apoptosis and autophagy in glioblastoma cells by targeting the p38 MAPK signalling pathway.

Background: Inhibition of p38 MAPK signalling leads to glioblastoma multiform (GBM) tumourigenesis. Nevertheless, the molecular mechanism that induces p38 MAPK signalling pathway silencing during GBM genesis has yet to be determined. Identifying new factors that can regulate p38 MAPK signalling is important for tumour treatment.

Hypoxia induced ferritin light chain (FTL) promoted epithelia mesenchymal transition and chemoresistance of glioma.

Background: Hypoxia, a fundamental characteristic of glioma, is considered to promote tumor malignancy by inducing process of epithelial mesenchymal transition (EMT). Ferritin Light Chain (FTL) is one of the iron metabolism regulators and is overexpressed in glioma. However, relationship between hypoxia and FTL expression and its role in regulating EMT remains unclear.

Small GTPase RHOE/RND3, a new critical regulator of NF-κB signalling in glioblastoma multiforme?

Objectives: Abnormal activation of NF-κB signalling is a major mechanism of apoptosis resistance in glioblastoma multiforme (GBM). Therefore, better understanding of the regulation of NF-κB signalling has a significant impact for GBM therapy. Here, we uncovered a critical role of the small GTPase RND3 in regulating the p65 subunit of NF-κB and NF-κB signalling in GBM.

GOLM1 silencing inhibits the proliferation and motility of human glioblastoma cells via the Wnt/β-catenin signaling pathway.

Golgi membrane protein 1 (GOLM1) is a type II transmembrane protein located in the cis- and medial-Golgi. Due to its function as an oncogene and proprotein convertase (PC) consensus site, GOLM1 will play a vital role in gene-targeted therapies and serve as a candidate tumor biomarker. However, few studies have explored its correlation with glioblastoma (GBM) progression.

Identification of differentially expressed key genes between glioblastoma and low-grade glioma by bioinformatics analysis.

Gliomas are a very diverse group of brain tumors that are most commonly primary tumor and difficult to cure in central nervous system. It's necessary to distinguish low-grade tumors from high-grade tumors by understanding the molecular basis of different grades of glioma, which is an important step in defining new biomarkers and therapeutic strategies. We have chosen the gene expression profile GSE52009 from gene expression omnibus (GEO) database to detect important differential genes.

PI3Kβ inhibitor AZD6482 exerts antiproliferative activity and induces apoptosis in human glioblastoma cells.

Glioblastoma is the most common type of primary brain tumour in adults, and its pathogenesis is particularly complicated. Among the many possible mechanisms underlying its pathogenesis, hyperactivation of the PI3K/Akt pathway is essential to the occurrence and development of glioma through the loss of PTEN or somatic activating mutations in PIK3CA. In the present study, we investigated the effect of the PI3Kβ inhibitor AZD6482 on glioma cells.

Identification of Core Biomarkers Associated with Outcome in Glioma: Evidence from Bioinformatics Analysis.

Glioma is the most common neoplasm of the central nervous system (CNS); the progression and outcomes of which are affected by a complicated network of genes and pathways. We chose a gene expression profile of GSE66354 from GEO database to search core biomarkers during the occurrence and development of glioma. A total of 149 samples, involving 136 glioma and 13 normal brain tissues, were enrolled in this article.

TGX-221 inhibits proliferation and induces apoptosis in human glioblastoma cells.

Glioblastoma is the most common type of primary brain tumor in adults, with high mortality and morbidity rates. More effective therapeutic strategies are imperative. Previous studies have shown that the known p110-β-selective inhibitor TGX-221 blocks the activation of PKB/Akt in PTEN-deficient cells.

SSRP1 silencing inhibits the proliferation and malignancy of human glioma cells via the MAPK signaling pathway.

Structure-specific recognition protein 1 (SSRP1) has been considered as a potential biomarker, since aberrant high expression of SSRP1 has been detected in numerous malignant tumors. However, the correlation between the expression level of SSRP1 and glioma remains unclear. The present study attempted to investigate the role of SSRP1 in the pathogenesis of glioma.

Revalidation and redescription of Brachymystax tsinlingensis Li, 1966 (Salmoniformes: Salmonidae) from China.

Brachymystax tsinlingensis Li, 1966 is revalidated and redescribed. It can be distinguished from all congeners by the following combination of characteristics: no spots on operculum; gill rakers 15-20; lateral-line scales 98-116; pyloric caeca 60-71. Unique morphological characters and genetic divergence of this species are discussed.

[Review on taxonomical studies of Chinese inland-water fish].

We reviewed the taxonomy and systematics research history of freshwater fish in China based on 1 236 taxonomic literature records on Chinese freshwater fish. The research was divided into five research periods according to specific historical events: (1) period by foreign scholars, (2) period with Chinese scholars, (3) period during World War II and Civil War, (4) recovery period and (5) period of rapid development. There were representative studies and innovations in all periods.