10/26/2024


Cigarette smoking could have certain effects on gut microbiota. Some pioneering studies have investigated effects of active smoking on the microbiome in local segments of the digestive tract, while active smoking-induced microbiome alterations in the whole digestive tract have not been fully investigated. Here, we developed a rat model of active smoking and characterized the effects of active smoking on the microbiota within multiple regions along the digestive tract. Blood glucose and some metabolic factors levels, the microbial diversity and composition, relative abundances of taxa, bacterial network correlations and predictive functional profiles were compared between the control group and active smoking group. We found that active smoking induced hyperglycemia and significant reductions in serum insulin and leptin levels. Active smoking induced region-specific shifts in microbiota structure, composition, network correlation and metabolism function along the digestive tract. Our results demonstrated that active smoking resulted in a reduced abundance of some potentially beneficial genera (i.e. Clostridium, Turicibacter) and increased abundance of potentially harmful genera (i.e. Desulfovibrio, Bilophila). Functional prediction suggested that amino acid, lipid, propanoate metabolism function could be impaired and antioxidant activity may be triggered. Active smoking may be an overlooked risk to health through its potential effects on the digestive tract microbiota, which is involved in the cause and severity of an array of chronic diseases.The complex and adaptive nature of malignant neoplasm constitute a major challenge for the development of effective anti-oncogenic therapies. Emerging evidence has uncovered the pivotal functions exerted by the small leucine-rich proteoglycans, decorin and biglycan, in affecting tumor growth and progression. In their soluble forms, decorin and biglycan act as powerful signaling molecules. By receptor-mediated signal transduction, both proteoglycans modulate key processes vital for tumor initiation and progression, such as autophagy, inflammation, cell-cycle, apoptosis, and angiogenesis. Despite of their structural homology, these two proteoglycans interact with distinct cell surface receptors and thus modulate distinct signaling pathways that ultimately affect cancer development. In this review, we summarize growing evidence for the complex roles of decorin and biglycan signaling in tumor biology and address potential novel therapeutic implications.Critical in revealing cell heterogeneity and identifying new cell subtypes, cell clustering based on single-cell RNA sequencing (scRNA-seq) is challenging. Due to the high noise, sparsity, and poor annotation of scRNA-seq data, existing state-of-the-art cell clustering methods usually ignore gene functions and gene interactions. In this study, we propose a feature extraction method, named FEGFS, to analyze scRNA-seq data, taking advantage of known gene functions. Specifically, we first derive the functional gene sets based on Gene Ontology (GO) terms and reduce their redundancy by semantic similarity analysis and gene repetitive rate reduction. Then, we apply the kernel principal component analysis to select features on each non-redundant functional gene set, and we combine the selected features (for each functional gene set) together for subsequent clustering analysis. To test the performance of FEGFS, we apply agglomerative hierarchical clustering based on FEGFS and compared it with seven state-of-the-art cnes related to these cell clusters.Glioma and pancreatic cancer are tumors with a high degree of malignancy, morbidity, and mortality. The present study explored possible molecular mechanisms and potential diagnostic and prognostic biomarker-PLPP4 of glioma and PAAD. PLPP4 is differentially elevated in glioma and PAAD tissues. Statistical analysis from TCGA demonstrated that high expression of PLPP4 significantly and positively correlated with clinicopathological features, including pathological grade and poor overall survival in glioma and PAAD patients. Following this, the methylation levels of PLPP4 also affected overall survival in clinical tissue samples. Silencing PLPP4 inhibited proliferation, invasion, and migration in LN229 cells and PANC-1 cells. Moreover, the combination of multiple proteins for the prognosis prediction of glioma and PAAD was evaluated. These results were conducted to elaborate on the potential roles of the biomarker-PLPP4 in clonability and invasion of glioma and PAAD cells.Adenoid cystic carcinoma (ACC) is a rare, basaloid, epithelial tumor, arising mostly from salivary glands. Radiation therapy can be employed as a single modality for unresectable tumors, in an adjuvant setting after uncomplete resection, in case of high-risk pathological features, or for recurrent tumors. Due to ACC intrinsic radioresistance, high linear energy transfer (LET) radiotherapy techniques have been evaluated for ACC irradiation while fast neutron therapy has now been abandoned due to toxicity concerns, charged particle beams such as protons and carbon ions are at present the beams used for hadron therapy. https://www.selleckchem.com/products/sodium-oxamate.html Carbon ion radiation therapy (CIRT) is currently increasingly used for ACC irradiation. The aim of this review is to describe the immunological, molecular and clinicopathological bases that support ACC treatment with CIRT, as well as to expose the current clinical evidence that reveal the advantages of using CIRT for treating ACC.
Renal cell carcinoma (RCC) associated with Xp11.2 translocation/
gene fusion is a rare and new subtype of RCC and was classified by the WHO in 2004. Since then, multiple 5' fusion partners for
have been reported; however, the impact of individual fusion variant on specific clinicopathologic features of Xp11.2 RCCs has not been well defined.

Four Xp11.2 translocation RCCs were identified by morphological, immunostaining, and fluorescence
hybridization (FISH) assays from 200 patients who attended Guangdong General Hospital between January 2017 and January 2020. All these four cases were further analyzed by RNA sequencing to explore their
gene fusion partners. The clinicopathologic features, including clinical manifestations, pathological findings, treatment strategies, clinical outcomes, and follow-up information on Xp11.2 translocation RCCs, were recorded and evaluated.

These four cases affected one male and three females. The median age was 13 years at the time of diagnosis (range = 4-20 years of Xp11.2 RCCs with specific
gene fusions. We identified a novel
-
fusion in Xp11.2 translocation RCCs for the first time, which has unique morphology and worse prognosis than those with other variant
rearrangements. Integration of morphological, immunohistochemical, and molecular methods is often necessary for the precise diagnosis and optimal clinical management of malignant tumors.
In conclusion, our data expand the list of TFE3 gene fusion partners and the clinicopathologic features of Xp11.2 RCCs with specific TFE3 gene fusions. We identified a novel VCP-TFE3 fusion in Xp11.2 translocation RCCs for the first time, which has unique morphology and worse prognosis than those with other variant TFE3 rearrangements. Integration of morphological, immunohistochemical, and molecular methods is often necessary for the precise diagnosis and optimal clinical management of malignant tumors.
The purpose of the study is to explore the potential competing endogenous RNA (ceRNA) network and investigate the molecular mechanism of long noncoding RNA (lncRNA)
(
) in hepatocellular carcinoma (HCC)development.

By analyzing the data of HCC in The Cancer Genome Atlas (TCGA) database, we included differentially expressed lncRNA and microRNA (miRNA) profiles and constructed ceRNA networks related to the prognosis of HCC patients. qRT-PCR, Western blotting, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), transwell assay, and the nude mouse model were employed to test the effects of
and
on tumor proliferation and growth
and
.

In the study, we identified 115 messenger RNAs (mRNAs), 12 lncRNAs, and 37 miRNAs by intersecting differentially expressed genes (DEGs) in TCGA and StarBase databases. Then,
-
-
pathway came into notice after further survival analysis and hub gene screening. Our results showed that
expression was upregulated significantly in HCC tissues and cell lines. Downregulation of both
, the target of
in HCC, and
inhibited tumor proliferation and growth
and
. Furthermore,
could regulate
expression through binding to
in HCC cell lines.

is a promising prognostic factor in HCC, and the
-
-
axis may be a potential therapeutic target for HCC.
SNHG1 is a promising prognostic factor in HCC, and the SNHG1-miR-326-LMNB2 axis may be a potential therapeutic target for HCC.Over 90% of potential anti-cancer drug candidates results in translational failures in clinical trials. The main reason for this failure can be attributed to the non-accurate pre-clinical models that are being currently used for drug development and in personalised therapies. To ensure that the assessment of drug efficacy and their mechanism of action have clinical translatability, the complexity of the tumor microenvironment needs to be properly modelled. 3D culture models are emerging as a powerful research tool that recapitulates in vivo characteristics. Technological advancements in this field show promising application in improving drug discovery, pre-clinical validation, and precision medicine. In this review, we discuss the significance of the tumor microenvironment and its impact on therapy success, the current developments of 3D culture, and the opportunities that advancements that in vitro technologies can provide to improve cancer therapeutics.
Brain metastases (BMs) are associated with poor prognosis and significant mortality, and approximately 25% of patients with non-small cell lung cancer (NSCLC) develop BMs. The present study was aimed to understand the relationships between BM and NSCLC and reveal potential biomarkers and therapeutic targets in NSCLC-related BM.

The differentially expressed genes (DEGs) expressed during NSCLC and BM development were predicted by bioinformatics analysis, and the expression of the upstream transcription factor nuclear factor of activated T cells (NFAT) was confirmed as a differential gene expressed in both NSCLC and BM. In addition, the expression of proteins encoded by these DEGs was verified by immunohistochemical experiments examining normal lung tissue, lung cancer tissue, and brain metastasis tissue from 30 patients with NSCLC related BM.

The co-DEGs interleukin (IL)-11, cadherin 5 (CDH5) and C-C motif chemokine 2 (CCL2) link NSCLC and BM in the Gene Expression Omnibus (GEO) database, and NFAT may target the expression of these co-DEGs. In the GEO database, NFATc1 and NFATc3 were significantly downregulated in NSCLC tissues (P <.05), whereas NFATc1, NFATc2, NFATc3, and NFATc4 were significantly downregulated in BMs (P <.05). Consistent findings were observed in the immunohistochemical analysis.

NFATc1 and NFATc3 may play important roles in the occurrence of NSCLC and BM by regulating IL-11, CDH5, and CCL2.
NFATc1 and NFATc3 may play important roles in the occurrence of NSCLC and BM by regulating IL-11, CDH5, and CCL2.