[MEtabolic reprogramming in cancer]
Dynamic changes in metabolic pathways can arise from genetic mutations and growth signals within cancer microenvironments. This leads to heightened biosynthesis and abnormal bioenergetics, fostering cell proliferation, metastasis, survival, and evasion of immune destruction. Additionally, metabolic remodeling plays a role in regulating tumor epigenetic alterations by influencing the activity of epigenetic modification enzymes and gene expression in cancer. Consequently, targeting cancer metabolism emerges as a promising avenue for effective cancer therapies. Our primary focus in investigating the role of cancer metabolism revolves around understanding the mechanisms of metabolic reprogramming, particularly in response to hypoxic environmental stress, oncogenic growth signaling, and cancer stem cells
[Mitochondrial Dynamics in cancer]
Mitochondria are dynamic organelles, constantly undergoing fusion and division in response to various stimuli. Precise regulation at multiple levels is necessary for these processes, enabling the cell to synchronize mitochondrial activity with nutrient availability, biosynthetic demands, proliferation rates, and external stimuli. The functions of these organelles are intricately connected to their morphology. Our research delves into the detailed molecular roles of changes in mitochondrial dynamics in cancer, with a specific focus on various molecules related to mitochondrial dynamics and their correlation with tumor progression.
[REplication Stress response]
DNA Replication is a meticulously regulated process ensuring the accurate duplication of the genome once per cell cycle. Any condition compromising this process is termed replication stress, a major contributor to genome instability associated with pre-tumor and tumor cells. Oncogenes often induce alterations in replication timing and progression, leading to replication stress. In order to become cancerous, cells need to upregulate the replication stress response. Our research focuses on understanding the molecular mechanisms through which cancer reduces replication stress, a critical step in initiating the oncogenic process.
[Cell to cell COMMUNICATION in tumor microenvironment ]
Exosomes, specialized membrane-enclosed extracellular vesicles ranging from 50 to 150 nm, play a crucial role in intercellular communication by carrying proteins, RNAs, DNA, lipids, and metabolites. They have the ability to reprogram recipient cells, influencing various biological processes in health and disease. In cancer, exosomes have emerged as key mediators facilitating communication between cancer cells and the local/distant microenvironment, crucial for tumor growth and systemic dissemination. Tumor-derived exosomes alter the tumor microenvironment, promoting processes like tumor growth, neovascularization, immune escape, and metastatic progression, including the formation of premetastatic niches. Beyond a higher release rate, exosomal content from tumors significantly differs from that of normal cells. Our research focuses on understanding the molecular mechanisms governing exosome production, content, and their functional roles in cancer behavior.