Expression Profile
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ORL ◽  
2021 ◽  
pp. 1-8
Shizhi He ◽  
Abdeyrim Arikin ◽  
Jiaming Chen ◽  
Tianqiao Huang ◽  
Zhen Wu ◽  

<b><i>Introduction:</i></b> Papillary thyroid microcarcinoma (PTMC) is a specific subgroup of papillary thyroid carcinoma and defined with the dimension ≤1 cm by the WHO. Although it shows a relatively high 10-year livability, the metastasis of PTMC into other tissues and organs seriously affects the daily life of patients with relatively high mortality. Therefore, the genetic basis for the metastasis of PTMC needs to be explored for effective therapeutic targets. Here, we conducted a series of comparative analysis of the transcriptional expression profile between PTMC patients with and without lymph node metastasis. <b><i>Methods:</i></b> Gene expression profile and gene function were analyzed using RNA extracted from pathological tissues of 12 patients with PTMC, and the core biomarkers closely related to its metastasis were identified. <b><i>Results:</i></b> Our results showed that 7,507 genes and 42 RNAs showed remarkably different expression patterns. More sophisticated analysis showed that the high expression of 2 lncRNAs (T077499 and T004533) resulted in the metastasis of PTMC, which suggests that the expression pattern of the 2 lncRNAs may act as a potential biomarker for pathogenesis and prognosis of PTMC metastasis. <b><i>Conclusion:</i></b> Our findings preliminarily reveal the molecular mechanisms for PTMC metastasis, which will provide vital reference for subsequent studies about the genetic basis and molecular targeted therapy for PTMC metastasis.

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Weishuang Ma ◽  
Jiaming Liang ◽  
Junjian Mo ◽  
Siyuan Zhang ◽  
Ningdong Hu ◽  

Abstract Background Lung adenocarcinoma (LUAD) is the most prevalent non-small cell lung cancer (NSCLC). Patients with LUAD have a poor 5-year survival rate. The use of immune checkpoint inhibitors (ICIs) for the treatment of LUAD has been on the rise in the past decade. This study explored the prognostic role of butyrophilin-like 9 (BTNL9) in LUAD. Methods Gene expression profile of buytrophilins (BTNs) was determined using the GEPIA database. The effect of BTNL9 on the survival of LUAD patients was assessed using Kaplan-Meier plotter and OncoLnc. Correlation between BTNL9 expression and tumor-infiltrating immune cells (TILs) was explored using TIMER and GEPIA databases. Further, the relationship between BTNL9 expression and drug response was evaluated using CARE. Besides, construction and evaluation of nomogram based on BTNL9 expression and TNM stage. Results BTNL9 expression was downregulated in LUAD and was associated with a poor probability of 1, 3, 5-years overall survival (OS). In addition, BTNL9 expression was regulated at epigenetic and post-transcriptional modification levels. Moreover, BTNL9 expression was significantly positively correlated with ImmuneScore and ESTIMATEScore. Furthermore, BTNL9 expression was positively associated with infiltration levels of B cells, CD4+ T cells, and macrophages. Kaplan-Meier analysis showed that BTNL9 expression in B cells and dendritic cells (DCs) was significantly associated with OS. BTNL9 expression was significantly positively correlated with CARE scores. Conclusions These findings show that BTNL9 is a potential prognostic biomarker for LUAD. Low BTNL9 expression levels associated with low infiltration levels of naïve B cells, and DCs in the tumor microenvironment are unfavorable for OS in LUAD patients.

2021 ◽  
Vol 12 ◽  
Xiao Liu ◽  
Jinran Lin ◽  
Hao Wu ◽  
Yilun Wang ◽  
Lin Xie ◽  

Objective: The mechanism of CD4+ T-cell dysfunction in systemic lupus erythematosus (SLE) has not been fully understood. Increasing evidence show that long noncoding RNAs (lncRNAs) can regulate immune responses and take part in some autoimmune diseases, while little is known about the lncRNA expression and function in CD4+ T of SLE. Here, we aimed to detect the expression profile of lncRNAs in lupus CD4+ T cells and explore the mechanism that how lincRNA00892 in CD4+ T cells is involved in the pathogenesis of SLE.Methods: The expression profiles of lncRNAs and mRNAs in CD4+ T cells from SLE patients and healthy controls were detected by microarray. LincRNA00892 and CD40L were chosen for validation by quantitative real-time PCR (qRT-PCR). Coexpression network was conducted to predict the potential target genes of lincRNA00892. Then lincRNA00892 was overexpressed in normal CD4+ T cells via lentivirus transfection. The expression of lincRNA00892 was detected by qRT-PCR. The expression of CD40L was detected by qRT-PCR, western blotting, and flow cytometry, respectively. The expression of CD69 and CD23 was measured by flow cytometry. The secretion of IgG was determined by enzyme-linked immunosorbent assay (ELISA). The proteins targeted by lincRNA00892 were measured by RNA pulldown and subsequent mass spectrometry (MS). The interaction between heterogeneous nuclear ribonucleoprotein K (hnRNP K) and lincRNA00892 or CD40L was detected by RNA immunoprecipitation (RIP) assay.Results: A total of 1887 lncRNAs and 3375 mRNAs were found to be aberrantly expressed in CD4+ T cells of SLE patients compared to healthy controls. LincRNA00892 and CD40L were confirmed to be upregulated in CD4+ T cells of SLE patients by qRT-PCR. The lncRNA–mRNA coexpression network analysis indicated that CD40L was a potential target of lincRNA00892. Overexpression of lincRNA00892 enhanced CD40L protein levels while exerting little influence on CD40L mRNA levels in CD4+ T cells. In addition, lincRNA00892 could induce the activation of CD4+ T cells. Furthermore, lincRNA00892 led to the activation of B cells and subsequent secretion of IgG in a CD4+ T-cell–dependent manner. Finally, hnRNP K was found to be among the proteins pulled down by lincRNA00892, and hnRNP K could bind to lincRNA00892 or CD40L directly.Conclusion: Our results showed that the lncRNA expression profile was altered in CD4+ T cells of SLE. LincRNA00892 possibly contributed to the pathogenesis of SLE by targeting hnRNP K and subsequently upregulating CD40L expression to activate CD4+ T and B cells. These provided us a potential target for further mechanistic studies of SLE pathogenesis.

2021 ◽  
Vol 43 (1) ◽  
Meenu Sharma ◽  
V. Verma ◽  
Narendra K. Bairwa

Abstract Background Stress response is mediated by the transcription of stress-responsive genes. The F-box motif protein Saf1p is involved in SCF-E3 ligase mediated degradation of the adenine deaminase, Aah1p upon nutrient stress. The four transcription regulators, BUR6, MED6, SPT10, SUA7, are listed for SAF1 in the genome database of Saccharomyces cerevisiae. Here in this study, we carried out an in-silico analysis of gene expression and transcription factor databases to understand the regulation of SAF1 expression during stress for hypothesis and experimental analysis. Result An analysis of the GEO profile database indicated an increase in SAF1 expression when cells were treated with stress agents such as Clioquinol, Pterostilbene, Gentamicin, Hypoxia, Genotoxic, desiccation, and heat. The increase in expression of SAF1 during stress conditions correlated positively with the expression of RLM1, encoding the Rlm1p transcription factor. The expression of AAH1 encoding Aah1p, a Saf1p substrate for ubiquitination, appeared to be negatively correlated with the expression of RLM1 as revealed by an analysis of the Yeastract expression database. Based on analysis of expression profile and regulatory association of SAF1 and RLM1, we hypothesized that inactivation of both the genes together may contribute to stress tolerance. The experimental analysis of cellular growth response of cells lacking both SAF1 and RLM1 to selected stress agents such as cell wall and osmo-stressors, by spot assay indicated stress tolerance phenotype similar to parental strain however sensitivity to genotoxic and microtubule depolymerizing stress agents. Conclusions Based on in-silico and experimental data we suggest that SAF1 and RLM1 both interact genetically in differential response to genotoxic and general stressors.

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Dongyu Wu ◽  
Guangcong Zhang ◽  
Jiamei Ma ◽  
Hongfen Wu ◽  
Ju Xiong ◽  

Background. Accumulating evidence has suggested that Nei-like DNA glycosylase 3 (NEIL3) is associated with human tumors. However, there are few studies on the role of NEIL3 in hepatocellular carcinoma (HCC). The aim of this study was to investigate the expression profile of NEIL3 and its clinical relevance in HCC. Materials and Methods. A total of 130 HCC and corresponding nontumor tissues were collected to perform immunohistochemistry (IHC). The clinical relevance and prognostic value of NEIL3 in HCC were analyzed by the chi-square test, Kaplan–Meier analysis, the Cox proportional hazard model, and nomogram. Results. IHC showed that the NEIL3 protein level was remarkably upregulated in tumor tissues compared with nontumor tissues (fold change = 1.24; P < 0.001 ). High NEIL3 expression was significantly correlated with BCLC stage ( P = 0.004 ) and TNM stage ( P = 0.005 ). Overall survival (OS) and disease-free survival (DFS) rates in the high NEIL3 expression group were significantly worse than those in the low NEIL3 expression group ( P = 0.007 and P = 0.004 , respectively). Furthermore, subgroup analysis showed that high NEIL3 expression predicted worse OS and DFS for HCC patients with advanced TNM stage, poorly differentiated tumor, HBsAg positive, or cirrhosis. Multivariate analysis and the prognostic nomograms revealed that tumor NEIL3 level may serve as a promising prognostic indicator for OS and DFS in HCC patients. Conclusion. Our findings suggested that NEIL3 might be a potential prognosis assessment marker and therapeutic target for HCC patients.

Genome ◽  
2021 ◽  
Ayse Gokce Keskus ◽  
Melike Tombaz ◽  
Burcin Irem Arici ◽  
Fatma Betul Dincaslan ◽  
Afshan Nabi ◽  

Human Angiotensin I Converting Enzyme 2 (ACE2) plays essential roles in blood pressure regulation and SARS-CoV-2 entry. ACE2 has a highly conserved, one-to-one ortholog, called ace2, in zebrafish, which is an important model for human diseases. However, zebrafish ace2 expression profile has not yet been studied during early development, between genders, across different genotypes, or in disease. Moreover, a network-based meta-analysis for the extraction of functionally enriched pathways associated with differential ace2 expression is lacking in the literature. Herein, we first identified significant development-, tissue-, genotype- and gender-specific modulations in ace2 expression via meta-analysis of zebrafish Affymetrix transcriptomics datasets (ndatasets=107); and the correlation analysis of ace2 meta-differential expression profile revealed distinct positively and negatively correlated local functionally enriched gene networks. Moreover, we demonstrated that ace2 expression was significantly modulated under different physiological and pathological conditions related to development, tissue, gender, diet, infection, and inflammation using additional RNAseq datasets. Our findings implicate a novel translational role for zebrafish ace2 in organ differentiation and pathologies observed in the intestines and liver.

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