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<p>Cancer cells often remodel their catabolic processes to support proliferation, growth, survival, and progression. This study investigated the transcriptional dysregulation of choline catabolism genes in pan-cancer, using TCGA and mRNA expression profiles from liver cancer cohorts. The studies revealed that choline catabolic genes, including choline kinase A, choline kinase B, choline dehydrogenase, and choline phosphotransferase, were prominently activated in stage-specific hepatocellular carcinoma (HCC) liver tumors with significant p-values (p &lt; 0.0001). Additionally, these genes were further analyzed for their ontological functionality, showing that they play a crucial role in the biosynthesis of phosphatidylcholine, essential for membrane synthesis during cell proliferation and survival. Furthermore, ROC curve analysis demonstrated greater specificity and sensitivity for these genes in stage-specific HCC tumors with significant area under the curve values. Overall survival studies also confirmed that these genes were associated with poor survival in HCC patients with significant p-values (p &lt; 0.05). Gene effect score analysis revealed higher negative scores for choline catabolic genes in liver tumor cell lines. Moreover, integrative genomic drug sensitivity studies identified a negative correlation with this catabolism, highlighting potential therapeutic targets such as Bryostatin1, Amuvatinib, FH535, Linsitinib, and DMOG. These findings could pave the way for the use of targeted therapies that focus on choline catabolic dysregulation in HCC treatment.</p>

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The transcriptional dysregulation of choline catabolism genes was implicated in HCC stage-specific carcinogenesis

  • 期刊论文

  • 发表日期：

    2025年1月29日

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  • Karthik Balakrishnan

摘要

Cancer cells often remodel their catabolic processes to support proliferation, growth, survival, and progression. This study investigated the transcriptional dysregulation of choline catabolism genes in pan-cancer, using TCGA and mRNA expression profiles from liver cancer cohorts. The studies revealed that choline catabolic genes, including choline kinase A, choline kinase B, choline dehydrogenase, and choline phosphotransferase, were prominently activated in stage-specific hepatocellular carcinoma (HCC) liver tumors with significant p-values (p < 0.0001). Additionally, these genes were further analyzed for their ontological functionality, showing that they play a crucial role in the biosynthesis of phosphatidylcholine, essential for membrane synthesis during cell proliferation and survival. Furthermore, ROC curve analysis demonstrated greater specificity and sensitivity for these genes in stage-specific HCC tumors with significant area under the curve values. Overall survival studies also confirmed that these genes were associated with poor survival in HCC patients with significant p-values (p < 0.05). Gene effect score analysis revealed higher negative scores for choline catabolic genes in liver tumor cell lines. Moreover, integrative genomic drug sensitivity studies identified a negative correlation with this catabolism, highlighting potential therapeutic targets such as Bryostatin1, Amuvatinib, FH535, Linsitinib, and DMOG. These findings could pave the way for the use of targeted therapies that focus on choline catabolic dysregulation in HCC treatment.