Abstract 2408: Targeted bioinformatics analysis identifies highABATtranscript expression as a multi-cancer marker of favorable patient prognosis

2021 ◽  
Author(s):  
Erika L. Knott ◽  
Nancy J. Leidenheimer
Keyword(s):  
Bioinformatics Analysis ◽  
Cancer Marker ◽  
Patient Prognosis

scholarly journals DNAJB4 identified as a potential breast cancer marker: evidence from bioinformatics analysis and basic experiments

Gland Surgery ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1955-1972
Author(s):  
Linlong Mo ◽  
Jiayou Liu ◽  
Ziquan Yang ◽  
Xun Gong ◽  
Fanlun Meng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Bioinformatics Analysis ◽  
Cancer Marker ◽  
Basic Experiments

scholarly journals ROR1 Potentiates FGFR Signaling in Basal-Like Breast Cancer

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 718 ◽  
Author(s):  
Gaurav Pandey ◽  
Nicholas Borcherding ◽  
Ryan Kolb ◽  
Paige Kluz ◽  
Wei Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Biochemical Analysis ◽  
Bioinformatics Analysis ◽  
Orphan Receptor ◽  
Potential Therapeutic Target ◽  
Immunodeficient Mice ◽  
Basal Like Breast Cancer ◽  
Cancer Types ◽  
Patient Prognosis ◽  
Aggressive Subtype

Among all breast cancer types, basal-like breast cancer (BLBC) represents an aggressive subtype that lacks targeted therapy. We and others have found that receptor tyrosine kinase-like orphan receptor 1 (ROR1) is overexpressed in BLBC and other types of cancer and that ROR1 is significantly correlated with patient prognosis. In addition, using primary patient-derived xenografts (PDXs) and ROR1-knockout BLBC cells, we found that ROR1+ cells form tumors in immunodeficient mice. We developed an anti-ROR1 immunotoxin and found that targeting ROR1 significantly kills ROR1+ cancer cells and slows down tumor growth in ROR1+ xenografts. Our bioinformatics analysis revealed that ROR1 expression is commonly associated with the activation of FGFR-mediated signaling pathway. Further biochemical analysis confirmed that ROR1 stabilized FGFR expression at the posttranslational level by preventing its degradation. CRISPR/Cas9-mediated ROR1 knockout significantly reduced cancer cell invasion at cellular levels by lowering FGFR protein and consequent inactivation of AKT. Our results identified a novel signaling regulation from ROR1 to FGFR and further confirm that ROR1 is a potential therapeutic target for ROR1+ BLBC cells.

scholarly journals High miR-139-3p expression predicts a better prognosis for hepatocellular carcinoma: a pooled analysis

2018 ◽  
Vol 47 (1) ◽  
pp. 383-390 ◽  
Author(s):  
Yu Zhu ◽  
Chengmao Zhou ◽  
Qixiong He
Keyword(s):  
Hepatocellular Carcinoma ◽  
Target Genes ◽  
Bioinformatics Analysis ◽  
Pooled Analysis ◽  
Micro Rna ◽  
The Cancer Genome Atlas ◽  
Analysis Tool ◽  
Patient Prognosis ◽  
Liver Hepatocellular Carcinoma ◽  
Cancer Tissues

Objective To observe the expression and clinical significance of micro RNA (miR)-139-3p in liver cancer tissues, and to explore its relationship with miR-139-3p target genes related to the prognosis of hepatocellular carcinoma (HCC). Methods A total of 362 patients with HCC were included in the study. Liver hepatocellular carcinoma data were obtained directly from The Cancer Genome Atlas data portal .The bioinformatics analysis tool TargetScan was applied to predict miR-139-3p target genes. Results Survival time was significantly higher in patients with high miR-139-3p expression, compared with the low miR-139-3p expression group. Bioinformatics analysis showed that miR-139-3p target genes ISG20L2, RAD54B, KIAA0101, and PIGS were significantly negatively correlated with miR-139-3p expression. Conclusions High miR-139-3p expression in HCC tissues was indicative of good patient prognosis. miR-139-3p target genes ISG20L2, RAD54B, KIAA0101, and PIGS were related to HCC prognosis.

scholarly journals Role of the CBX Molecular Family in Lung Adenocarcinoma Tumorigenesis and Immune Infiltration

2021 ◽  
Vol 12 ◽  
Author(s):  
Chun Zhang ◽  
Lisha Chang ◽  
Yizhen Yao ◽  
Ce Chao ◽  
Zhongchun Ge ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Bioinformatics Analysis ◽  
Immune Cell ◽  
Diagnostic Value ◽  
Promoting Effect ◽  
Receiver Operating Characteristic Curves ◽  
Kaplan Meier ◽  
And Migration ◽  
Patient Prognosis

Background: The members of the Chromobox (CBX) family are important epigenetic regulatory molecules with critical biological roles in many tumors. However, no study has analyzed or verified their role in lung adenocarcinoma (LUAD).Methods: UALCAN and Oncomine databases were used to analyze CBX expression in LUAD, and the cBioPortal database was used to analyze CBX genetic variations. The Kaplan-Meier plotter and UALCAN databases were used to identify molecules with prognostic value. Gene Ontology pathway, receiver operating characteristic curves, and tumor-infiltrating immune cell analyses were used to clarify the biological function of the CBX hub molecules. Paired tumor samples and lung adenocarcinoma cell lines were collected for molecular functional assays to validate the results of the bioinformatics analysis.Results: CBX3/5 may have a cancer-promoting effect and its expression is associated with a poor patient prognosis, while CBX7 shows an opposite trend. CBX3/5/7 can regulate signaling pathways, regulate tumor immune cell infiltration, and has diagnostic value. Molecular biology experiments show that CBX3/5 is highly expressed in LUAD patients; in vitro it promotes the proliferation and migration of the LUAD cell line and can regulate the expression of the corresponding cytokines. CBX7 has opposite effects.Conclusion: Our bioinformatics analysis and subsequent experimental verification confirmed the CBX family members acted as hub signaling molecules in LUAD. The results provide new potential targets for the diagnosis and treatment of this cancer.

scholarly journals CAF-induced placental growth factor facilitates neoangiogenesis in hepatocellular carcinoma

2019 ◽  
Vol 52 (1) ◽  
pp. 18-25 ◽  
Author(s):  
Zhongjian Liu ◽  
Mingmei Chen ◽  
Rongce Zhao ◽  
Yuan Huang ◽  
Fei Liu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Growth Factor ◽  
Bioinformatics Analysis ◽  
Placental Growth Factor ◽  
The Cancer Genome Atlas ◽  
Cancer Associated Fibroblasts ◽  
Interactive Analysis ◽  
The Third ◽  
Cancer Genome Atlas ◽  
Patient Prognosis

Abstract As a highly malignant tumor, hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. In most HCC patients, the development of HCC begins with hepatitis, which is followed by fibrosis and cirrhosis before progressing to HCC. Cancer-associated fibroblasts (CAFs), which are generally believed to be derived from activated hepatic stellate cells (HSCs), are highly involved in the development of HCC through the secretion of cytokines and angiogenic factors. The results of our study showed that a considerable number of CAFs highly expressed CD90 and were enriched in HCC tissues. Bioinformatics analysis of the transcriptome of HCC tissues revealed that placental growth factor (PlGF) is significantly correlated with CD90 expression. The isolated primary CAFs and activated HSCs overexpressed PlGF and CD90. In addition, the results of gene expression profiling interactive analysis based on The Cancer Genome Atlas showed that high levels of both PlGF and CD90 are correlated with tumor angiogenesis markers (CD31, CD34, and CD105) and predict poor HCC patient prognosis. In summary, our results suggest that CAFs can generate PlGF and may provide an effective target for CAFs-regulated neoangiogenesis in HCC.

TAp73 opposes tumor angiogenesis by promoting hypoxia-inducible factor 1α degradation

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Cancer Progression ◽  
Hypoxia Inducible Factor ◽  
Tumor Hypoxia ◽  
Human Lung Cancer ◽  
Regulatory Subunit ◽  
Patients With Cancer ◽  
Hypoxia Inducible Factor 1 ◽  
Chemically Induced ◽  
Induced Tumors ◽  
Patient Prognosis

Tumor hypoxia and hypoxia-inducible factor 1 (HIF-1) activationare associated with cancer progression. Here, we demonstrate thatthe transcription factor TAp73 opposes HIF-1 activity through anontranscriptional mechanism, thus affecting tumor angiogenesis.TAp73-deficient mice have an increased incidence of spontaneousand chemically induced tumors that also display enhanced vascularization.Mechanistically, TAp73 interacts with the regulatory subunit(α) of HIF-1 and recruits mouse double minute 2 homolog intothe protein complex, thus promoting HIF-1α polyubiquitination andconsequent proteasomal degradation in an oxygen-independentmanner. In human lung cancer datasets, TAp73 strongly predictsgood patient prognosis, and its expression is associated with lowHIF-1 activation and angiogenesis. Our findings, supported by invivo and clinical evidence, demonstrate a mechanism for oxygenindependentHIF-1 regulation, which has important implicationsfor individualizing therapies in patients with cancer.

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