Essential oils (EOs) and hydrolates (Hds) are natural sources of biologically active ingredients with broad applications in the cosmetic industry. In this study, nationally produced (mainland Portugal and Azores archipelago) EOs (11) and Hds (7) obtained from forest logging and thinning of Eucalyptus globulus, Pinus pinaster, Pinus pinea and Cryptomeria japonica, were chemically evaluated, and their bioactivity and sensorial properties were assessed. EOs and Hd volatiles (HdVs) were analyzed by GC-FID and GC-MS. 1,8-Cineole was dominant in E. globulus EOs and HdVs, and α- and β-pinene in P. pinaster EOs. Limonene and α-pinene led in P. pinea and C. japonica EOs, respectively. P. pinaster and C. japonica HVs were dominated by α-terpineol and terpinen-4-ol, respectively. The antioxidant activity was determined by DPPH, ORAC and ROS. C. japonica EO showed the highest antioxidant activity, whereas one of the E. globulus EOs showed the lowest. Antimicrobial activity results revealed different levels of efficacy for Eucalyptus and Pinus EOs while C. japonica EO showed no antimicrobial activity against the selected strains. The perception and applicability of emulsions with 0.5% of EOs were evaluated through an in vivo sensory study. C. japonica emulsion, which has a fresh and earthy odour, was chosen as the most pleasant fragrance (60%), followed by P. pinea emulsion (53%). In summary, some of the studied EOs and Hds showed antioxidant and antimicrobial activities and they are possible candidates to address the consumers demand for more sustainable and responsibly sourced ingredients.
According to the SEER program of NCI, lung, and bronchus cancer are the second most common cancer with an estimated 236,740 diagnoses in 2022. Fifty-four percent of the patients are expected to die of the disease in the United States alone. The five-year overall survival rate for these cancers is 22.9 percent. Lung adenocarcinoma (LUAD) accounts for forty percent of all lung cancer cases in the United States. Genetic biomarker-based early detection and precision treatment of LUAD patients can play a critical role in the reduction of the mortality rate. The purpose of this investigation was to use an integrated bioinformatics approach to identify differentially expressed Hub genes in LUAD with > 10 connections in the genetic interaction network(s). The higher number of genetic interactions potentially suggests their important role in patient survival. Out of 23,483 genes from seven published cancer studies and databases, we identified 107 significantly altered (up or down-regulated) genes that are common to all data sources. The Database for Annotation, Visualization, and Integrated Discovery (DAVID) showed that many of the identified 107 genes were involved in DNA replication, DNA repair, ATP binding, and cancer pathways. A protein-protein interaction network was mapped with the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING). This analysis revealed 1116 protein-to-protein interactions (PPI) among the 107 genes. We selected 25 genes, which exhibited >30 PPI interactions each which showed Cox coefficients for gene expression, where a positive coefficient corresponds to a worse survival rate with higher levels of gene expression, while a negative coefficient corresponds to a better prognosis with lower levels of gene expression; it also provided a False Discovery Rate (FDR) with a corrected p-value. The Kaplan-Meier survival curves for genes that had an FDR of below 0.05 were graphed inside of the OncoLnc tool. Patients were subclassified into the low- and high-Hub gene expression level groups if the median expression was in the bottom 25 percentile or top 25 percentile. Hub genes isolated from Cytoscape were entered into OncoLnc to collect data on the relationship between LUAD patients (n=492) survival and gene expression, which resulted in the identification of three genes, Checkpoint Kinase 1, Cyclin E1, and Exonuclease 1. All three genes showed a significant correlation between increased differential expression in LUAD and worsened patient survival. These signature Hub genes (Checkpoint Kinase 1, Cyclin E1, and Exonuclease 1) and associated genetic networks can potentially be developed as early diagnostic markers or targets in precision gene therapies for improved prognosis of LUAD patients. Citation Format: Prateek Gupta, Leya Joykutty, Diaaidden Alwadi, Ana Ruas, Deodutta Roy, Quentin Felty, Alok Deoraj. Checkpoint Kinase I, Cyclin E1, and Exonuclease I genes play role in the survival of lung adenocarcinoma patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3158.
Ovarian cancer is the most lethal gynecological cancer, accounting for thousands of cancer-related deaths in the United States every year. Though there has been progress towards understanding ovarian cancer pathogenesis, much is not yet understood about the molecular mechanisms that facilitate chemoresistance and metastasis. Our work has shown that nuclear respiratory factor 1 (NRF1) is highly active in several human cancers, though the role of NRF1 remains largely unexplored in ovarian carcinomas. Therefore, our aim was to examine the role of this transcription factor in ovarian cancer, since understanding its transcriptional landscape may reveal NRF1 or its target genes as possible therapeutic targets for this highly aggressive cancer. The Cancer Genome Atlas (TCGA) was utilized to collect RNA-Seq data from 379 serous cystadenocarcinoma samples, where we found that about 20% of ovarian cancer patients had altered NRF1 expression, showing either high expression or amplification of this transcription factor. Patients with high NRF1 expression were found to have decreased survival compared to patients with low NRF1 expression. NRF1 amplification was also correlated with the overamplification of one of its target genes - Jrk helix-turn-helix protein (JRK) in 26% of the samples. JRK regulates centrosome amplification, and through the production of mitotic spindle abnormalities, centrosome amplification contributes to genomic instability. Further investigation of the relationship between NRF1 and JRK uncovered that protein levels of JRK and β-catenin were significantly higher in NRF1-induced stem-like cells compared to the control group, and JRK is known to bind to β-catenin. Our NRF1 ChIP-Seq analyses showed that promoters of these two genes - JRK and CTNNB1 - were bound to NRF1. The Flow Assorted Cell Sorting (FACS), ChIP-Seq, RNA Seq and confocal microscopic studies suggest that through JRK, NRF1 regulates β-catenin transcriptional activity. Amplified gene expression is the one of the first steps towards oncogene activation, and our findings illustrate that altered NRF1 expression (i.e., overexpression or amplification) coupled with that of JRK influences the prognosis of patients diagnosed with ovarian cancer. The Wnt/β-catenin pathway is also highly active in the aggressive ovarian cancer. In addition to JRK, through the activation of β-catenin, NRF1may also affect the development of ovarian tumors. Taken together, our findings provide a novel insight into the molecular basis of the contribution of NRF1-driven JRK-mediated β-catenin transcriptional activity to the susceptibility of highly aggressive ovarian cancer. A better understanding of how ovarian neoplasm formation depends on NRF1-JRK-β-catenin pathway may open new avenues for therapeutic strategy against ovarian cancer. Citation Format: Ana Ruas, Quentin Felty, Jayanta K. Das, Alok Deoraj, Changwon Yoo, Deodutta Roy. A NRF1-driven JRK-mediated β-catenin transcriptional activity contributes to the aggressive growth of ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 779.
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