: CDCA5 has been reported as a gene involved in the cell cycle, however current research provides little details. Our goal was to figure out its functions and probable mechanisms in pan-cancer. : Pan-cancer bulk sequencing data and web-based analysis tools were applied to analyze CDCA5's correlations with the gene expression, clinical prognosis, genetic alterations, promoter methylation, alternative splicing, immune checkpoints, tumor microenvironment and enrichment. Real‑time PCR, cell clone formation assay, CCK-8 assay, cell proliferation assay, migration assay, invasion assay and apoptosis assay were used to evaluate the effect of CDCA5 silencing on colon cancer cell lines. : CDCA5 is highly expressed in most tumors, which has been linked to a poor prognosis. Immune checkpoints analysis revealed that CDCA5 was associated with the immune gene CD276 in various tumors. Single-cell analysis showed that CDCA5 correlated with proliferating T cell infiltration in COAD. Enrichment analysis demonstrated that CDCA5 may modify cell cycle genes to influence p53 signaling. The examination of DLD1 cells revealed that CDCA5 increased the proliferation and blocked cell apoptosis. : This study contributes to the knowledge of the role of CDCA5 in carcinogenesis, highlighting the prognostic potential and carcinogenic involvement of CDCA5 in pan-cancer.
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http://dx.doi.org/10.7150/jca.91082 | DOI Listing |
Sci Rep
January 2025
Drug Discovery Program, Ontario Institute for Cancer Research, Toronto, ON, M5G 0A3, Canada.
High mortality and low response rates in lung cancer patients call for novel therapeutic targets. Data mining of whole-genome genetic dependency screens suggest Cell Division Cycle 40 (CDC40) to be an essential protein for lung cancer cell survival. We characterized CDC40 knockdown effects in multiple lung cancer cell lines, revealing induced cell cycle defects that resulted in strong growth inhibition and activation of apoptosis.
View Article and Find Full Text PDFFront Mol Biosci
December 2024
Department of Urology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Background: Cancer stem cells are characterized by self-renewal, clonal tumor initiation capacity, and treatment resistance, which play essential roles in the tumor progression of prostate cancer (PCa). In this study, we aim to explore the features of cancer stemness and characterize the expression of stem cell-related genes for PCa.
Methods: We downloaded RNA-seq data and related clinical information from The Cancer Genome Atlas (TCGA) database.
Biochem Pharmacol
December 2024
Center for Drug Discovery, Graduate School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka 422-8526, Japan. Electronic address:
The discovery of new small-molecule inhibitors is essential to enhancing our understanding of biological events at the molecular level and driving advancements in drug discovery. Mitotic inhibitors have played a crucial role in development of anticancer drugs. Beyond traditional microtubule inhibitors, various inhibitors targeting specific mitotic factors have been developed.
View Article and Find Full Text PDFHeliyon
December 2024
Department of Advanced Toxicology Research, Korea Institute of Toxicology, Daejeon, 34114, Republic of Korea.
Background: Xenogeneic transplantation induces acute graft-versus-host disease (aGvHD) and subsequent vital organ damage. Herein, we aimed to examine hepatic damage associated with aGvHD using histopathology and gene expression profiles.
Methods: A xenografic GvHD model was established by engrafting human peripheral blood mononuclear cells (PBMCs) into immunodeficient NOD-scid IL2Rγnull (NSG) mice after busulfan conditioning.
Comput Struct Biotechnol J
December 2024
Key Laboratory of Computer-Aided Drug Design of Dongguan City, The First Dongguan Affiliated Hospital, School of Pharmacy, Guangdong Medical University, Dongguan 523710, China.
Background: Digestive system malignancies, including esophageal carcinoma (ESCA), stomach adenocarcinoma (STAD), liver hepatocellular carcinoma (LIHC), and colon adenocarcinoma (COAD), pose significant global health challenges. Identifying shared and distinct regulatory mechanisms across these cancers can lead to improved therapies. This study aims to construct and compare competing endogenous RNA (ceRNA) networks across ESCA, STAD, LIHC, and COAD to identify RNA biomarkers that could serve as precision therapeutic targets to enhance clinical outcomes and advance personalized cancer care.
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