scholarly journals SPAG5 Expression Correlated With Prognostic Implication and Immune Infiltration in Lung Adenocarcinoma

2022 ◽  
Author(s):  
Jianjiang Xie ◽  
Xie Xu ◽  
Huaping Zhou
Keyword(s):  
Lung Adenocarcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Underlying Mechanism ◽  
Immune Checkpoints ◽  
Dna Damage And Repair ◽  
Mesenchymal Transition ◽  
Immune Infiltration ◽  
Kaplan Meier ◽  
Associate Antigen ◽  
Cd4 Cell

Abstract Background Sperm-associate antigen 5 (SPAG5) is a critical oncogene in several cancers. But the role of SPAG5A in lung adenocarcinoma (LUAD) remains unclear. Thus, the aims of our study are to explore the function and underlying mechanism of SPAG5 in LUAD. Methods Expression of SPAG5 was determined using the Oncomine, TIMER, and GEPIA databases. Correlation of SPAG5 and survival was detected by GEPIA database, PrognoScan, Kaplan-Meier Plotter databases. And the association between SPAG5 and tumor malignant phenotypes were analyzed by the CancerSEA. Besides, the correlation between SPAG5 expression and tumor immune infiltration as well as immune checkpoints were analyzed by TIMER. the co-expression genes of SPAG5 were identified using STRING, and the mutation and biological function of SPAG5 and its co-expression genes were determined by cBioPortal and Metascape, respectively. Finally, the SPAG5 expression in LUAD samples was determined by tissues microarrays (TMA) and immunohistochemistry (IHC) analyses.Results We found that upregulated SPAG5 associated with poor survival of LUAD patients. Besides, SPAG5 expression associated to B cell, CD4+ cell, CD8+ cell, macrophage, DC cell as well as CD274, CTLA4, GZMB, LAG3, PDCD1, TIGIT in LUAD. SPAG5 expression also associated with cell proliferation, cell cycle, DNA damage and repair, epithelial-mesenchymal transition (EMT), invasion, and stemness, inflammation in LUAD. Conclusion Our finding indicated that SPAG5 acted as a crucial oncogene in LUAD, and correlated with unfavorable survival as well as tumor infiltration inflation.

scholarly journals Co-Expression of Coxsackievirus/Adenovirus Receptors and Desmoglein 2 in Lung Adenocarcinoma: A Comprehensive Analysis of Bioinformatics and Tissue Microarrays

2020 ◽  
Vol 9 (11) ◽  
pp. 3693
Author(s):  
Ching-Fu Weng ◽  
Chi-Jung Huang ◽  
Mei-Hsuan Wu ◽  
Henry Hsin-Chung Lee ◽  
Thai-Yen Ling
Keyword(s):  
Overall Survival ◽  
Survival Analysis ◽  
Lung Adenocarcinoma ◽  
Cox Regression ◽  
Epithelial Mesenchymal Transition ◽  
Early Stage ◽  
The Cancer Genome Atlas ◽  
Cancer Tissue ◽  
Mesenchymal Transition ◽  
Kaplan Meier

Introduction: Coxsackievirus/adenovirus receptors (CARs) and desmoglein-2 (DSG2) are similar molecules to adenovirus-based vectors in the cell membrane. They have been found to be associated with lung epithelial cell tumorigenesis and can be useful markers in predicting survival outcome in lung adenocarcinoma (LUAD). Methods: A gene ontology enrichment analysis disclosed that DSG2 was highly correlated with CAR. Survival analysis was then performed on 262 samples from the Cancer Genome Atlas, forming “Stage 1A” or “Stage 1B”. We therefore analyzed a tissue microarray (TMA) comprised of 108 lung samples and an immunohistochemical assay. Computer counting software was used to calculate the H-score of the immune intensity. Cox regression and Kaplan–Meier analyses were used to determine the prognostic value. Results: CAR and DSG2 genes are highly co-expressed in early stage LUAD and associated with significantly poorer survival (p = 0.0046). TMA also showed that CAR/DSG2 expressions were altered in lung cancer tissue. CAR in the TMA was correlated with proliferation, apoptosis, and epithelial–mesenchymal transition (EMT), while DSG2 was associated with proliferation only. The Kaplan–Meier survival analysis revealed that CAR, DSG2, or a co-expression of CAR/DSG2 was associated with poorer overall survival. Conclusions: The co-expression of CAR/DSG2 predicted a worse overall survival in LUAD. CAR combined with DSG2 expression can predict prognosis.

scholarly journals Analysis of the role of METTL5 as a hub gene in lung adenocarcinoma based on a weighted gene co-expression network

2021 ◽  
Vol 18 (5) ◽  
pp. 6608-6619
Author(s):  
Xinwang Yan ◽  
◽  
Xiaowen Zhao ◽  
Qing Yan ◽  
Ye Wang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Differential Expression ◽  
Epithelial Mesenchymal Transition ◽  
Differential Expression Analysis ◽  
Predictive Performance ◽  
Tumor Stage ◽  
Malignant Progression ◽  
Mesenchymal Transition ◽  
Kaplan Meier ◽  
Differential Expression Genes

<abstract> <p>Lung adenocarcinoma (LUAD) is a frequently diagnosed malignant tumor that is highly invasive and lethal. The prognosis of patients with LUAD still needs to be improved, as conventional treatment is remarkably well tolerated. In this study, the expression profile of LUAD in the TCGA database was used for differential expression analysis, and differential expression genes were determined to construct a weighted gene co-expression network analysis (WGCNA) for dividing and finding the gene modules with the highest correlation with tumor stage. Here, METTL5, DDX23, GPSM2, CEP95, WDCP, and METL17 were identified as hub genes. According to the relation degree, METTL5 was determined as the candidate gene in this study. Difference analysis and receiver operating characteristic (ROC) curve were applied to identify the predictive performance of METTL5 in LUAD, and Kaplan-Meier (KM) analysis showed that the prognosis of LUAD patients with high METTL5 expression was poor. Further GSEA analysis showed that high-expressed METTL5 was related to epithelial-mesenchymal transition and other pathways. Therefore, METTL5 may be involved in the occurrence and malignant progression of LUAD. The current findings provide an effective molecular target for early diagnosis of LUAD, helping monitor the malignant progression of LUAD and improve the prognosis of LUAD patients.</p> </abstract>

scholarly journals A Comprehensive Analysis of Potential Gastric Cancer Prognostic Biomarker ITGBL1 Associated With Immune Infiltration and Epithelial–mesenchymal Transition

2021 ◽  
Author(s):  
Zhe Wang ◽  
Liu Fu ◽  
Junjie Zhang ◽  
Yanli Ge ◽  
Cheng Guo ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Immunohistochemical Analysis ◽  
Migration And Invasion ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
Immune Infiltration ◽  
Kaplan Meier ◽  
Bioinformatics Databases ◽  
Kaplan Meier Plotter ◽  
Tgf Β1

Abstract Background: Integrin, beta-like 1 (ITGBL1) is involved in a variety of human malignancies. However, the information on the involvement of ITGBL1 in gastric carcinoma (GC) is limited. Hence, this study aimed to further explore the functions and mechanisms of ITGBL1 in GC. Methods: First, multiple bioinformatics databases, including Oncomine, Timer, UALCAN, and Kaplan–Meier Plotter, were used to predict the expression level and prognostic value of ITGBL1, as well as its association with immune infiltration and epithelial–mesenchymal transition (EMT) in GC. Quantitative reverse transcription–polymerase chain reaction and immunohistochemical analysis were used to to detect the expression of ITGBL1 in both GC tissues and cells. Then, targeted silencing of ITGBL1 in GC cells was further to examine the biological functions of ITGBL1.Results: These databases revealed that ITGBL1 was overexpressed and affected the overall survival in GC. Besides, the expression of ITGBL1 positively correlated with immune-infiltrating cells and EMT-related markers. Subsequently, molecular biology experiments verified these predictions. In GC tissues and cells, ITGBL1 was notably overexpressed. Loss-of-function studies showed that the knockdown of ITGBL1 significantly suppressed migration and invasion but promoted apoptosis in MGC803 GC cells. Furthermore, the inhibition of ITGBL1 resulted in remarkably increased protein expression levels of cadherin 1 (CDH1), while the expression of Vimentin, Snail, and TGF-β1 was downregulated, indicating the initiation and progression of GC caused by ITGBL1 partly via inducing EMT. Conclusion: To sum up, the findings indicated that ITGBL1 acted as a valuable oncogenic factor in GC.

COPS8 in cutaneous melanoma: an oncogene that accelerates the malignant development of tumor cells and predicts poor prognosis

2020 ◽  
Vol 85 (2) ◽  
pp. 242-250
Author(s):  
Liangliang Sun
Keyword(s):  
Cutaneous Melanoma ◽  
Epithelial Mesenchymal Transition ◽  
Underlying Mechanism ◽  
Cop9 Signalosome ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Kaplan Meier ◽  
Melanoma Cell Proliferation ◽  
Melanoma Patients ◽  
Related Proteins

ABSTRACT This study aimed to investigate the roles of COP9 signalosome subunit 8 (COPS8) and its underlying mechanism in cutaneous melanoma. Bioinformatics tools were utilized to analyze the expression of COPS8 in cutaneous melanoma, while Kaplan–Meier analysis was employed to assess the correlation between COPS8 and patients’ overall survival. The proliferation, migration, and invasion of cells were estimated by CCK8, colony formation, and Transwell assays. Western blot was used to check the expression of epithelial–mesenchymal transition (EMT)-related proteins. Results showed that COPS8 was up-regulated and predicted a poor clinical outcome for cutaneous melanoma patients. Knockdown of COPS8 inhibited cutaneous melanoma cell proliferation, migration and invasion, whereas overexpression of COPS8 resulted in the opposite outcomes. The up-regulation of E-cadherin and down-regulation of N-cadherin, vimentin, and snail were caused by silencing COPS8 while their expression showed contrary trends in cells with overexpressed COPS8. Collectively, COPS8 is up-regulated and promotes cutaneous melanoma progression via regulating EMT.

scholarly journals Overexpressed P75CUX1 promotes EMT in glioma infiltration by activating β-catenin

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Anqi Xu ◽  
Xizhao Wang ◽  
Jie Luo ◽  
Mingfeng Zhou ◽  
Renhui Yi ◽  
...  
Keyword(s):  
Epithelial Mesenchymal Transition ◽  
Tumor Grade ◽  
Prognostic Indicator ◽  
Migration And Invasion ◽  
Poor Overall Survival ◽  
Mesenchymal Transition ◽  
Kaplan Meier ◽  
Homeobox Protein

AbstractThe homeobox protein cut-like 1 (CUX1) comprises three isoforms and has been shown to be involved in the development of various types of malignancies. However, the expression and role of the CUX1 isoforms in glioma remain unclear. Herein, we first identified that P75CUX1 isoform exhibited consistent expression among three isoforms in glioma with specifically designed antibodies to identify all CUX1 isoforms. Moreover, a significantly higher expression of P75CUX1 was found in glioma compared with non-tumor brain (NB) tissues, analyzed with western blot and immunohistochemistry, and the expression level of P75CUX1 was positively associated with tumor grade. In addition, Kaplan–Meier survival analysis indicated that P75CUX1 could serve as an independent prognostic indicator to identify glioma patients with poor overall survival. Furthermore, CUX1 knockdown suppressed migration and invasion of glioma cells both in vitro and in vivo. Mechanistically, this study found that P75CUX1 regulated epithelial–mesenchymal transition (EMT) process mediated via β-catenin, and CUX1/β-catenin/EMT is a novel signaling cascade mediating the infiltration of glioma. Besides, CUX1 was verified to promote the progression of glioma via multiple other signaling pathways, such as Hippo and PI3K/AKT. In conclusion, we suggested that P75CUX1 could serve as a potential prognostic indicator as well as a novel treatment target in malignant glioma.

scholarly journals Upregulation of LINC01426 promotes the progression and stemness in lung adenocarcinoma by enhancing the level of SHH protein to activate the hedgehog pathway

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Xiaoli Liu ◽  
Zuwei Yin ◽  
Linping Xu ◽  
Huaimin Liu ◽  
Lifeng Jiang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Bioinformatics Analysis ◽  
Epithelial Mesenchymal Transition ◽  
Mrna Level ◽  
Hedgehog Pathway ◽  
Biological Processes ◽  
Protein Coding ◽  
Mesenchymal Transition ◽  
Functional Roles ◽  
Rip Assay

AbstractLong noncoding RNAs (lncRNAs) play crucial roles in regulating a variety of biological processes in lung adenocarcinoma (LUAD). In our study, we mainly explored the functional roles of a novel lncRNA long intergenic non-protein coding RNA 1426 (LINC01426) in LUAD. We applied bioinformatics analysis to find the expression of LINC01426 was upregulated in LUAD tissue. Functionally, silencing of LINC01426 obviously suppressed the proliferation, migration, epithelial–mesenchymal transition (EMT), and stemness of LUAD cells. Then, we observed that LINC01426 functioned through the hedgehog pathway in LUAD. The effect of LINC01426 knockdown could be fully reversed by adding hedgehog pathway activator SAG. In addition, we proved that LINC01426 could not affect SHH transcription and its mRNA level. Pull-down sliver staining and RIP assay revealed that LINC01426 could interact with USP22. Ubiquitination assays manifested that LINC01426 and USP22 modulated SHH ubiquitination levels. Rescue assays verified that SHH overexpression rescued the cell growth, migration, and stemness suppressed by LINC01426 silencing. In conclusion, LINC01426 promotes LUAD progression by recruiting USP22 to stabilize SHH protein and thus activate the hedgehog pathway.

The Impacts of Bone Marrow Mesenchymal Stem Cells (BMSCs)-Derived Periostin on Epithelial-Mesenchymal Transition (EMT) of Cervical Cancer Cells

2022 ◽  
Vol 12 (4) ◽  
pp. 820-826
Author(s):  
Chengyong Wu ◽  
Weifeng Wei ◽  
Jing Li ◽  
Shenglin Peng
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Signal Transduction Pathway ◽  
Underlying Mechanism ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Essential Components ◽  
Cervical Cancer Cells ◽  
E Cadherin

Epithelial-mesenchymal transition (EMT) is closely related to the migrating and invading behaviors of cells. Periostin is one of the essential components in the extracellular matrix and can induce EMT of cells and their sequential metastasis. But its underlying mechanism is unclear. The Hela and BMSC cell lines were assigned into Periostin-mimic group, Periostin-Inhibitor group and Periostin-NC group followed by analysis of cell migration and invasion, expression of E-Cadherin, Vimentin, β-Catenin, Snail, MMP-2, MMP-9, PTEN, and p-PTEN. Cells in Periostin-mimic group exhibited lowest migration, least number of invaded cells, as well as lowest levels of Vimentin, β-Catenin, Snail, MMP-2, MMP-9, p-PTEN, Akt, p-Akt, p-GSK-3β, p-PDK1 and p-cRcf, along with highest levels of E-cadherin and PTEN. Moreover, cells in Periostin-NC group had intermediate levels of these above indicators, while, the Periostin-Inhibitor group exhibited the highest migration rate, the most number of invaded cells, and the highest levels of these proteins (P < 0.05). In conclusion, BMSCs-derived Periostin can influence the EMT of cervical cancer cells possibly through restraining the activity of the PI3K/AKT signal transduction pathway, indicating that Periostin might be a target of chemotherapy in clinics for the treatment of cervical cancer.

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