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From Omics to Therapeutic Targets in Cancer 2.0

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Dear Colleagues,

Cancer is a complex genetic disease involving multiple pathways in its development and progression. Decades of research have helped in understanding some of the underlying mechanisms, but our understanding of the disease remains incomplete. In recent years, technological advancements such as various high-throughput omics methods have immensely helped in unraveling some of the unknown complexities of cancer. The integration of data obtained from different omics methods has further enhanced of our knowledge of diseases.

The main purpose of this Special Issue is to collect new research in the field of cancer biology. We invite the submission of all studies employing new and innovative ideas to understand the basic biology of cancer. This Special Issue is not limited to novel experimental approaches but also welcomes new computational methodologies developed in the field.

Dr. Prasoon Agarwal
Guest Editor

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Keywords

multi-omics
bioinformatics
cancer
data integration
novel methods development
therapeutic targets or biomarkers
epigenetics
genetics
single-cell omics

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Research

18 pages, 3209 KiB

Open AccessArticle

Apoptotic Effect of Gallic Acid via Regulation of p-p38 and ER Stress in PANC-1 and MIA PaCa-2 Cells Pancreatic Cancer Cells

by Jeong Woo Kim, Jinwon Choi, Moon Nyeo Park and Bonglee Kim

Int. J. Mol. Sci. 2023, 24(20), 15236; https://doi.org/10.3390/ijms242015236 - 16 Oct 2023

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Abstract

Pancreatic cancer (PC) is currently recognized as the seventh most prevalent cause of cancer-related mortality among individuals of both genders. It is projected that a significant number of individuals will succumb to this disease in the forthcoming years. Extensive research and validation have been conducted on both gemcitabine and 5-fluorouracil as viable therapeutic options for PC. Nevertheless, despite concerted attempts to enhance treatment outcomes, PC continues to pose significant challenges in terms of achieving effective treatment alone through chemotherapy. Gallic acid, an endogenous chemical present in various botanical preparations, has attracted considerable attention due to its potential as an anticancer agent. The results of the study demonstrated that gallic acid exerted a decline in cell viability that was dependent on its concentration. Furthermore, it efficiently suppressed cell proliferation in PC cells. This study observed a positive correlation between gallic acid and the production of reactive oxygen species (ROS). Additionally, it confirmed the upregulation of proteins associated with the protein kinase-like endoplasmic reticulum kinase (PERK) pathway, which is one of the pathways involved in endoplasmic reticulum (ER) stress. Moreover, the administration of gallic acid resulted in verified alterations in the transmission of mitogen-activated protein kinase (MAPK) signals. Notably, an elevation in the levels of p-p38, which represents the phosphorylated state of p38 MAPK was detected. The scavenger of reactive oxygen species (ROS), N-Acetyl-L-cysteine (NAC), has shown inhibitory effects on phosphorylated p38 (p-p38), whereas the p38 inhibitor SB203580 inhibited C/EBP homologous protein (CHOP). In both instances, the levels of PARP have been successfully reinstated. In other words, the study discovered a correlation between endoplasmic reticulum stress and the p38 signaling pathway. Consequently, gallic acid induces the activation of both the p38 pathway and the ER stress pathway through the generation of ROS, ultimately resulting in apoptosis. The outcomes of this study provide compelling evidence to support the notion that gallic acid possesses considerable promise as a viable therapeutic intervention for pancreatic cancer. Full article

(This article belongs to the Special Issue From Omics to Therapeutic Targets in Cancer 2.0)

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18 pages, 3225 KiB

Open AccessArticle

In Silico Gene Prioritization Highlights the Significance of Bone Morphogenetic Protein 4 (BMP4) Promoter Methylation across All Methylation Clusters in Colorectal Cancer

by Daša Jevšinek Skok and Nina Hauptman

Int. J. Mol. Sci. 2023, 24(16), 12692; https://doi.org/10.3390/ijms241612692 - 11 Aug 2023

Viewed by 1006

Abstract

The cytosine–phosphate–guanine (CpG) island methylator phenotype (CIMP) represents one of the pathways involved in the development of colorectal cancer, characterized by genome-wide hypermethylation. To identify samples exhibiting hypermethylation, we used unsupervised hierarchical clustering on genome-wide methylation data. This clustering analysis revealed the presence of four distinct subtypes within the tumor samples, namely, CIMP-H, CIMP-L, cluster 3, and cluster 4. These subtypes demonstrated varying levels of methylation, categorized as high, intermediate, and very low. To gain further insights, we mapped significant probes from all clusters to Ensembl Regulatory build 89, with a specific focus on those located within promoter regions or bound regions. By intersecting the methylated promoter and bound regions across all methylation subtypes, we identified a total of 253 genes exhibiting aberrant methylation patterns in the promoter regions across all four subtypes of colorectal cancer. Among these genes, our comprehensive genome-wide analysis highlights bone morphogenic protein 4 (BMP4) as the most prominent candidate. This significant finding was derived through the utilization of various bioinformatics tools, emphasizing the potential role of BMP4 in colorectal cancer development and progression. Full article

(This article belongs to the Special Issue From Omics to Therapeutic Targets in Cancer 2.0)

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