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Clear cell renal cell carcinoma (ccRCC) is a malignant tumor of the urinary system. To explore the potential mechanisms of DHODH in ccRCC, we analyzed its molecular characteristics using public databases. TCGA pan-cancer dataset was used to analyze DHODH expression in different cancer types and TCGA ccRCC dataset was used to assess differential expression, prognosis correlation, immune infiltration, single-gene, and functional enrichment due to DHODH. The GSCALite and CellMiner databases were employed to explore drugs and perform molecular docking analysis with DHODH. Protein-protein interaction networks and ceRNA regulatory networks of DHODH were constructed using multiple databases. The effect of DHODH on ccRCC was confirmed in vitro. DHODH was highly expressed in ccRCC. Immune infiltration analysis revealed that DHODH may be involved in regulating the infiltration of immunosuppressive cells such as Tregs. Notably, DHODH influenced ccRCC progression by forming regulatory networks with molecules, such as hsa-miR-26b-5p and UMPS and significantly enhanced the malignant characteristics of ccRCC cells. Several drugs, such as lapatinib, silmitasertib, itraconazole, and dasatinib, were sensitive to DHODH expression and exhibited strong molecular binding with it. Thus, DHODH may promote ccRCC progression and is a candidate effective therapeutic target for ccRCC.
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http://dx.doi.org/10.1038/s41598-024-62738-0 | DOI Listing |
Front Med (Lausanne)
August 2025
First Clinical Medical School, Gansu University of Chinese Medicine, Lanzhou, Gansu Province, China.
Background: Carbon-ion radiotherapy (CIRT) is an advanced form of high linear energy transfer (LET) radiotherapy that has demonstrated superior biological effectiveness compared to conventional photon therapy in the treatment of various malignancies; however, its role in gastric cancer remains unclear. Dihydroorotate dehydrogenase (DHODH), a key enzyme implicated in cancer progression, has been linked to tumor radiosensitivity. This study aims to investigate whether CIRT inhibits gastric cancer progression via the regulation of DHODH.
View Article and Find Full Text PDFBiochemistry
September 2025
Loyola University Chicago, Department of Chemistry and Biochemistry, 1068 W Sheridan Rd, Chicago, Illinois 60660, United States.
Dihydroorotate dehydrogenase 1B (DHOD1B) is one of several flavoproteins that utilize active half-sites. These enzymes have two flavin cofactors (FAD and FMN) that each interact with a specific reductant/oxidant substrate/product. Electrons gained at one-half-site must be transmitted to the other half-site and iron-sulfur centers between the flavin cofactors serve in this role.
View Article and Find Full Text PDFBiochem Pharmacol
August 2025
Department of Infectious Diseases, The Affiliated Hospital of Qingdao University, Qingdao Medical College, Qingdao University, Qingdao 266011, China. Electronic address:
Cervical carcinoma remains a major public health challenge due to its elevated incidence and mortality rates. Dihydroorotate dehydrogenase (DHODH) is a crucial enzyme in de novo pyrimidine biosynthesis and ferroptosis defense with a targetable susceptibility in cancer. However, effective inhibitors of DHODH and their potential application in cervical cancer therapy have not yet been explored.
View Article and Find Full Text PDFBr J Pharmacol
August 2025
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.
Background: Hepatocellular carcinoma (HCC), a globally prevalent malignancy with high mortality rates, presents an unmet need for innovative effective therapies.
Purpose: This study aimed to explore the antitumour potential of compound XD, a novel oridonin derivative, on HCC and its underlying mechanism.
Experimental Approach: The antitumour effects of compound XD were investigated in several HCC cells lines and mice models.
Bioorg Med Chem
August 2025
School of Life Sciences, Faculty of Medicine, Tianjin University, Tianjin 300354, China; Hangzhou Institute of Medicine, Chinese Academy of Science, Hangzhou 310018, China; School of Molecular Medicine, Hangzhou Institute for Advanced Study, UCAS, Hangzhou 310024, China. Electronic address: xfang@ic
Mitochondrial proteostasis is essential for tumorigenesis, and mitochondrial inner membrane proteins have emerged as meaningful targets due to their crucial functions in regulating apoptosis, maintaining oxidative phosphorylation, and influencing tumor initiation and progression. Targeted protein degradation (TPD) has garnered significant attention as a promising therapeutic approach. However, conventional TPD platforms relying on the ubiquitin-proteasome system or lysosomal pathways encounter inherent obstacles in targeting proteins sequestered within the mitochondrial compartment and cannot degrade mitochondrial inner membrane proteins.
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