In the tumor microenvironment, significant metabolic alterations manifest, prominently characterized by heightened levels of lactic acid and enhanced protein lactylation. Lactic acid, a byproduct of anaerobic glycolysis, accumulates within the tumor milieu, thereby accentuating its acidic milieu and facilitating tumor progression and immune evasion. Concurrently, lactylation, a consequential post-translational modification induced by lactic acid, instigates functional perturbations in proteins, thereby intricately influencing cellular pathways within the tumor microenvironment. This nonenzymatic modification mediated by lactic acid critically perturbs protein functionality and signaling cascades pivotal for sustaining tumor cell viability, proliferation, and metastasis.
Moreover, lactic acid and lactylation are also linked to changes in gene expression and genetic regulation within tumors. Elevated lactic acid levels can influence the expression of genes involved in metabolic pathways, stress responses, and tumor progression. For instance, lactylation of histones, a key component of chromatin, has been shown to affect gene expression by altering chromatin structure and accessibility. This modification can lead to changes in transcriptional programs that promote tumor cell survival and adaptation. Additionally, lactylation may impact the activity of transcription factors and co-regulators, further modulating gene expression in response to the acidic microenvironment.
Therefore, understanding the intricate roles of lactic acid and lactylation in tumor pathogenesis, particularly their impact on gene expression and genetic regulation, offers promising avenues for therapeutic intervention. Research efforts focus on unraveling their influence on tumor cell biology, tumor microenvironment interactions, immune cell dysfunction, and mechanisms of therapeutic resistance. Novel strategies targeting lactic acid accumulation or inhibiting lactylation processes hold potential for developing innovative therapeutic approaches against tumors by addressing these metabolic and epigenetic alterations.
This Research Topic aims to explore recent advancements in the understanding of lactic acid and lactylation in tumor, providing a platform for original research articles, reviews, clinical studies, and meta-analyses. Contributions investigating mechanisms, biomarkers, therapeutic targets, and clinical implications of lactic acid and lactylation in tumor are encouraged. Additionally, studies exploring the interplay between these metabolic alterations and other signalling pathways in tumor progression are welcomed to broaden insights into tumor biology and therapeutic strategies.
We welcome submissions of original research papers, reviews, data report, hypothesis & theory, methods, and opinions, including (but not limited to) research on the following sub-themes:
• Explore the biochemical pathways through which lactic acid affects chromatin structure and epigenetic modifications in tumor cells.
• Experimental studies elucidating the role of lactic acid and lactylation in epigenetic modifications within the context of tumor.
• Computational analyses or modeling studies exploring gene expression changes associated with lactylation in tumor.
• Clinical studies evaluating the prognostic or predictive value of metabolic markers related to lactic acid metabolism in tumor.
• Discuss implications for clinical management and potential therapeutic interventions targeting metabolic dysregulation in tumor.
• Analyze changes in gene expression profiles induced by lactic acid and lactylation, using high-throughput sequencing and bioinformatics approaches.
In the tumor microenvironment, significant metabolic alterations manifest, prominently characterized by heightened levels of lactic acid and enhanced protein lactylation. Lactic acid, a byproduct of anaerobic glycolysis, accumulates within the tumor milieu, thereby accentuating its acidic milieu and facilitating tumor progression and immune evasion. Concurrently, lactylation, a consequential post-translational modification induced by lactic acid, instigates functional perturbations in proteins, thereby intricately influencing cellular pathways within the tumor microenvironment. This nonenzymatic modification mediated by lactic acid critically perturbs protein functionality and signaling cascades pivotal for sustaining tumor cell viability, proliferation, and metastasis.
Moreover, lactic acid and lactylation are also linked to changes in gene expression and genetic regulation within tumors. Elevated lactic acid levels can influence the expression of genes involved in metabolic pathways, stress responses, and tumor progression. For instance, lactylation of histones, a key component of chromatin, has been shown to affect gene expression by altering chromatin structure and accessibility. This modification can lead to changes in transcriptional programs that promote tumor cell survival and adaptation. Additionally, lactylation may impact the activity of transcription factors and co-regulators, further modulating gene expression in response to the acidic microenvironment.
Therefore, understanding the intricate roles of lactic acid and lactylation in tumor pathogenesis, particularly their impact on gene expression and genetic regulation, offers promising avenues for therapeutic intervention. Research efforts focus on unraveling their influence on tumor cell biology, tumor microenvironment interactions, immune cell dysfunction, and mechanisms of therapeutic resistance. Novel strategies targeting lactic acid accumulation or inhibiting lactylation processes hold potential for developing innovative therapeutic approaches against tumors by addressing these metabolic and epigenetic alterations.
This Research Topic aims to explore recent advancements in the understanding of lactic acid and lactylation in tumor, providing a platform for original research articles, reviews, clinical studies, and meta-analyses. Contributions investigating mechanisms, biomarkers, therapeutic targets, and clinical implications of lactic acid and lactylation in tumor are encouraged. Additionally, studies exploring the interplay between these metabolic alterations and other signalling pathways in tumor progression are welcomed to broaden insights into tumor biology and therapeutic strategies.
We welcome submissions of original research papers, reviews, data report, hypothesis & theory, methods, and opinions, including (but not limited to) research on the following sub-themes:
• Explore the biochemical pathways through which lactic acid affects chromatin structure and epigenetic modifications in tumor cells.
• Experimental studies elucidating the role of lactic acid and lactylation in epigenetic modifications within the context of tumor.
• Computational analyses or modeling studies exploring gene expression changes associated with lactylation in tumor.
• Clinical studies evaluating the prognostic or predictive value of metabolic markers related to lactic acid metabolism in tumor.
• Discuss implications for clinical management and potential therapeutic interventions targeting metabolic dysregulation in tumor.
• Analyze changes in gene expression profiles induced by lactic acid and lactylation, using high-throughput sequencing and bioinformatics approaches.