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The acquired drug resistance has been regarded as a main barrier for the effective treatment of temozolomide (TMZ) in glioblastoma (GBM). MiR-126-3p is commonly down-regulated and exerts tumor-suppressive roles in kinds of human cancers, including GBM. This study was designed to investigate the functions and mechanisms of miR-126-3p in regulating TMZ resistance in GBM.
Accumulating evidence elucidates the biological significance of long non-coding RNA (lncRNAs) in tumorigenesis and development. FGD5 antisense RNA 1 (FGD5-AS1) was previously revealed as an oncogene in several types of malignancies. However, the roles of FGD5-AS1 in glioblastoma (GBM) and its potential molecular mechanisms remain unclear.
T-box transcription factor 15 (TBX15) is upregulated in a variety of tumors and has been reported to promote uncontrolled proliferation of tumor cells and induce tumor cells to avoid apoptosis, thus accelerating the malignant transformation of malignant tumors. However, the prognostic value of TBX15 in glioma and its relationship with immune infiltration remain unknown. In this study, we intended to explore the prognostic value of TBX15 and its link to glioma immune infiltration and examine TBX15 expression in pan-cancer using RNAseq data in TPM format from TCGA and GTEx. TBX15 mRNA and protein expressions in glioma cells and adjacent normal tissue were detected and compared by RT-qPCR and Western blot. The effect of TBX15 on survival was assessed by Kaplan-Meier Method. The correlation between TBX15 upregulation and the clinicopathological characteristics of glioma patients was assessed by using TCGA databases, and the relationship between TBX15 and other genes in glioma was evaluated by using TCGA data. The top 300 genes most significantly associated with TBX15 were selected to establish a PPI network through the STRING database. The relationship between TBX15 mRNA expression and immune cell infiltration was explored by using ssGSEA and the TIMER Database. It was found that TBX15 mRNA expression in glioma tissues was significantly higher than that in the adjacent normal tissues, and this difference was most obvious in high-grade gliomas. TBX15 expression was increased in human gliomas and associated with worse clinicopathological characteristics and poorer survival prognosis in glioma patients. In addition, elevated TBX15 expression was linked to a collection of genes involved in immunosuppression. In conclusion, TBX15 played an important role in immune cell infiltration in glioma and may prove to be a predictor of the prognosis in glioma patients.
Gliomas, a prevalent form of primary brain tumors, are linked with a high mortality rate and unfavorable prognoses. Disulfidptosis, an innovative form of programmed cell death, has received scant attention concerning disulfidptosis-related lncRNAs (DRLs). The objective of this investigation was to ascertain a prognostic signature utilizing DRLs to forecast the prognosis and treatment targets of glioma patients.
Long non-coding RNAs (LncRNAs) have been demonstrated to play a vital role in human carcinogenesis. HOXA cluster antisense RNA 2 (HOXA-AS2), a 1048-bp lncRNA located between the HOXA3 and HOXA4 genes, is identified as an oncogene in several malignancies, including glioma. However, the biological functions of HOXA-AS2 and its underlying molecular mechanisms in glioma progression remain to be investigated.
Coronary atherosclerosis (CA) is the most common type of atherosclerosis. However, the inherent pathogenesis and mechanisms of CA are unclear, and the relationship with ferroptosis-related genes (FRGs) has not been reported. The purpose of this study was to use bioinformatics techniques to evaluate potential therapeutic targets for CA.Please provide the given name for author "Dingshun".Please provide the given name for author "Dingshun".
To investigate the effects of Reference cement (RC) and Belite cement (LC) systems, different molecular structures of polycarboxylate ether (PCE) were prepared through the free radical polymerization reaction and designated as PC-1 and PC-2. The PCE was characterized and tested using a particle charge detector, gel permeation chromatography, a rotational rheometer, a total organic carbon analyzer, and scanning electron microscopy. The results showed that compared to PC-2, PC-1 exhibited higher charge density and better molecular structure extension, with smaller side-chain molecular weight and molecular volume. PC-1 demonstrated enhanced adsorption capacity in cement, improved initial dispersibility of cement slurry, and a reduction in slurry yield stress of more than 27.8%. LC, with its higher C2S content and smaller specific surface area compared to RC, could decrease the formation of flocculated structures, resulting in a reduction in slurry yield stress of over 57.5% and displaying favorable fluidity in cement slurry. PC-1 had a greater retarding effect on the hydration induction period of cement compared to PC-2. RC, which had a higher C3S content, could adsorb more PCE, leading to a greater retarding effect on the hydration induction period compared to LC. LC and PC-2, on the other hand, exhibited inhibition during the hydration acceleration period. The addition of PCE with different structures did not significantly affect the morphology of hydration products in the later stage, which was consistent with the trend of KD variation. This indicates that the analysis of hydration kinetics can better reflect the final hydration morphology.
Cholestasis is a pathological state that leads to serious liver disease; however, therapeutic options remain limited. Yinchen and Gancao are often used in combination at different ratios in traditional Chinese formulae for the treatment of jaundice and cholestasis. In the present study, we investigated the effect of decoctions containing different ratios of Yinchen and Gancao (YGD) on alpha-naphthyl isothiocyanate (ANIT)-treated intrahepatic cholestasis (IC) in mice, and further explored the underlying mechanism. Treatment with 0:4 and 1:4 YGD significantly reduced plasma total bile acid (TBA), total bilirubin (TBIL), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) activities; decreased unconjugated and conjugated bile acid levels; and improved hepatocyte necrosis and inflammatory cells recruitment to hepatic sinusoids. Moreover, the expression levels of Toll-like receptor 4 (TLR4), interleukin-1β (IL-1β), IL-6, tumor necrosis factor alpha (TNF-α), C-C ligand 2 (CCL2), and C-X-C ligand 2 (CXCL2) in the liver were significantly reduced. However, treatment with 4:1 and 4:0 YGD increased plasma TBA, TBIL, AST, ALT, and ALP activities and aggravated liver cell injury and inflammation. Moreover, the mRNA expression of the bile salt export pump (BSEP) in the liver was significantly increased in mice treated with 4:0 YGD. The present study demonstrates that YGD containing a high proportion of Gancao, which inhibits the TLR4/NF-κB pathway and reduces the inflammatory response, had protective effects against ANIT-treated IC in mice. However, YGD containing a high proportion of Yinchen aggravated the ANIT-treated IC in mice, which may be related to upregulation of BSEP and boosting bile acid regurgitation from damage cholangiocytes to liver in ANIT-treated IC mice.
Long non-coding RNA small nucleolar RNA host gene 5 (lncRNA SNHG5) has been reported to participate in the occurrence and development of glioma. However, the function and underlying molecular mechanisms of SNHG5 in glioma remain largely unknown. The expressions of SNHG5, microRNA-1297 (miR-1297) and karyopherin subunit alpha 2 (KPNA2) in glioma tissues and cells were evaluated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) or western blot. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry were used to detect cell viability and apoptosis, respectively. Western blot was also performed to detect the expressions of autophagy-associated proteins. The relationship among lncRNA SNHG5, miR-1297 and KPNA2 was verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. SNHG5 and KPNA2 were over expressed, and the level of miR-1297 was down-regulated in glioma tissues and cell lines. Knockdown of SHNG5 promoted apoptosis, while suppressing cell viability and autophagy of A172 and LN340 cells. Meanwhile, SHNG5 harbored the binding sites with miR-1297, and a negative correlation between the expression of SNHG5 and miR-1297 in glioma tissues was also observed. Interestingly, silencing of miR-1297 undermined the SHNG5 depletion-mediated effect on cell viability, apoptosis, and autophagy. KPNA2 was a direct target of miR-1297, and negatively regulated by miR-1297. More importantly, gain of KPNA2 mitigated the effect of SHNG5l knockdown on glioma cells. Silencing of SNHG5 had an implication in inhibiting apoptosis and stimulating cell viability and autophagy by the miR-1297/KPNA2 axis in glioma.
Background: Glioma patients often experience unfavorable outcomes and elevated mortality rates. Our study established a prognostic signature utilizing cuproptosis-associated long non-coding RNAs (CRLs) and identified novel prognostic biomarkers and therapeutic targets for glioma. Methods: The expression profiles and related data of glioma patients were obtained from The Cancer Genome Atlas, an accessible online database. We then constructed a prognostic signature using CRLs and evaluated the prognosis of glioma patients by means of Kaplan-Meier survival curves and receiver operating characteristic curves. A nomogram based on clinical features was employed to predict the individual survival probability of glioma patients. Functional enrichment analysis was conducted to identify crucial CRL-related enriched biological pathways. The role of LEF1-AS1 in glioma was validated in two glioma cell lines (T98 and U251). Results: We developed and validated a prognostic model for glioma with 9 CRLs. Patients with low-risk had a considerably longer overall survival (OS). The prognostic CRL signature may serve independently as an indicator of prognosis for glioma patients. In addition, functional enrichment analysis revealed significant enrichment of multiple immunological pathways. Notable differences were observed between the two risk groups in terms of immune cell infiltration, function, and immune checkpoints. We further identified four drugs based on their different IC50 values from the two risk groups. Subsequently, we discovered two molecular subtypes of glioma (cluster one and cluster two), with the cluster one subtype exhibiting a remarkably longer OS compared to the cluster two subtype. Finally, we observed that inhibition of LEF1-AS1 curbed the proliferation, migration, and invasion of glioma cells. Conclusion: The CRL signatures were confirmed as a reliable prognostic and therapy response indicator for glioma patients. Inhibition of LEF1-AS1 effectively suppressed the growth, migration, and invasion of gliomas; therefore, LEF1-AS1 presents itself as a promising prognostic biomarker and potential therapeutic target for glioma.
This study addresses the lack of systematic investigation into the prognostic value of hand-crafted radiomic features derived from diffusion tensor imaging (DTI) in isocitrate dehydrogenase (IDH) wild-type glioblastoma (GBM), as well as the limited understanding of the biological interpretation of individual DTI radiomic features and metrics.
Gliomas are the most aggressive type of malignant brain tumors. Recent studies have demonstrated that the existence of glioma stem cells (GSCs) is critical for glioma recurrence, metastasis, and chemo- or radio-therapy resistance. Temozolomide (TMZ) has been used as an initial therapy for gliomas. However, the overall survival time is still limiting due to the lack of effective targets and treatment options. Therefore, identifying novel biomarkers for gliomas, especially for GSCs, is important to improve the clinical outcome in the future. In this study, we identify a human-specific long non-coding RNA (lncRNA, ENSG00000250377), termed GSCAR (glioma stem cell associated lncRNA), which is highly expressed in glioma cancerous tissues and cell lines. We reveal that GSCAR positively correlates with tumor grade. Glioma patients with GSCAR high expression exhibit shortened overall survival time, compared to patients with GSCAR low expression. Furthermore, we show that GSCAR knockdown by shRNAs or antisense oligonucleotide (ASO) reduces tumor cell proliferation, migration and xenograft tumor formation abilities. Mechanistic study shows that GSCAR acts as a ceRNA (competing endogenous RNA) for miR-6760-5p to promote the expression of oncogene SRSF1 (serine and arginine rich splicing factor 1). In addition, GSCAR mediates the protein complex formation between DHX9 (DExH-Box helicase 9) and IGF2BP2 (insulin-like growth factor 2 mRNA-binding protein 2), leading to the stabilization of SOX2 (sex-determining region Y-box 2) mRNA and then the transcriptional activation of GSCAR. Depleting GSCAR reduces SOX2 expression and GSC self-renewal ability, but promotes tumor cell responses to TMZ. These findings uncover that GSCAR/miR-6760-5p/SRSF1 axis and GSCAR/DHX9-IGF2BP2/SOX2 positive feedback loop are critical for glioma progression, which could be used as prognostic biomarkers and therapeutic targets in the future.
Glioma is characterized by high morbidity, high mortality, and poor prognosis. Despite tremendous advances in the treatment of glioma, the prognosis of patients with glioma is still unsatisfactory. There is an urgent need to discover novel molecular markers that effectively predict prognosis in patients with glioma. The investigation of the role of WEE2-AS1 in various tumors is an emerging research field, but the biological function and prognostic value of WEE2-AS1 in glioma have rarely been reported. This study aimed to assess the value of WEE2-AS1 as a potential prognostic marker of glioma.
Current diagnosis of glioma types requires combining both histological features and molecular characteristics, which is an expensive and time-consuming procedure. Determining the tumor types directly from whole-slide images (WSIs) is of great value for glioma diagnosis. This study presents an integrated diagnosis model for automatic classification of diffuse gliomas from annotation-free standard WSIs. Our model is developed on a training cohort (n = 1362) and a validation cohort (n = 340), and tested on an internal testing cohort (n = 289) and two external cohorts (n = 305 and 328, respectively). The model can learn imaging features containing both pathological morphology and underlying biological clues to achieve the integrated diagnosis. Our model achieves high performance with area under receiver operator curve all above 0.90 in classifying major tumor types, in identifying tumor grades within type, and especially in distinguishing tumor genotypes with shared histological features. This integrated diagnosis model has the potential to be used in clinical scenarios for automated and unbiased classification of adult-type diffuse gliomas.
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