Revathy Nadhan

Cancer remains a leading cause of morbidity and mortality worldwide, and effective strategies for cancer prevention are urgently needed to complement therapeutic advances. While dietary factors are known to influence cancer risk, the molecular mechanisms that mediate inter-individual responses to nutritional exposures remain poorly defined. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of gene expression, chromatin organization, metabolic homeostasis, immune signaling, and cellular stress responses, the core processes that drive cancer initiation and progression and are highly sensitive to nutritional status. In parallel, advances in precision nutrition have highlighted how variability in genetics, metabolism, microbiome composition, and epigenetic landscapes shape dietary influences on cancer susceptibility. This review integrates these rapidly evolving fields by positioning lncRNAs as molecular conduits that translate dietary exposures into transcriptional and epigenetic programs governing cancer development, progression, and therapeutic vulnerability. We provide mechanistic evidence demonstrating how dietary bioactive compounds and micronutrients, including polyphenols [such as curcumin, resveratrol, epigallocatechin gallate (EGCG)], flavonoids, alkaloids such as berberine, omega-3 (ω-3) fatty acids, folate, vitamin D, probiotic metabolites (such as butyrate and propionate), and trace elements (such as selenium and zinc), modulate oncogenic and tumor-suppressive lncRNAs. These nutrient–lncRNA interactions influence cancer-relevant pathways controlling proliferation, epithelial–mesenchymal transition (EMT), inflammation, oxidative stress, and metabolic rewiring. We further discuss emerging lncRNA signatures that reflect nutritional and metabolic states, their potential utility as biomarkers for individualized dietary interventions, and their integration into liquid biopsy platforms. Leveraging multi-omics datasets and systems biology, we outline AI-driven frameworks to map nutrient–lncRNA regulatory networks and identify targetable nodes for cancer chemoprevention. Finally, we address translational challenges, including compound bioavailability, inter-individual variability, and limited clinical validation, and propose future directions for incorporating lncRNA profiling into precision nutrition-guided cancer prevention trials. Together, these insights position lncRNAs at the nexus of diet and cancer biology and establish a foundation for mechanistically informed precision nutrition strategies in cancer chemoprevention.

Cancer remains a leading cause of morbidity and mortality worldwide, and effective strategies for cancer prevention are urgently needed to complement therapeutic ad-vances. While dietary factors are known to influence cancer risk, the molecular mecha-nisms that mediate inter-individual responses to nutritional exposures remain poorly defined. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of gene expression, chromatin organization, metabolic homeostasis, immune signaling, and cellular stress responses, core processes that drive cancer initiation and progression and are highly sensitive to nutritional status. In parallel, advances in pre-cision nutrition have highlighted how variability in genetics, metabolism, microbiome composition, and epigenetic landscapes shapes dietary influences on cancer susceptibility. This review integrates these rapidly evolving fields by positioning lncRNAs as molecular conduits that translate dietary exposures into transcriptional and epigenetic programs governing cancer development, progression, and therapeutic vulnerability. We provide mechanistic evidence demonstrating how dietary bioactive compounds and micronu-trients, including polyphenols (curcumin, resveratrol, EGCG), flavonoids, alkaloids such as berberine, omega-3 fatty acids, folate, vitamin D, probiotic metabolites (such as bu-tyrate and propionate), and trace elements (such as selenium, and zinc), modulate on-cogenic and tumor-suppressive lncRNAs. These nutrient-lncRNA interactions influence cancer-relevant pathways controlling proliferation, epithelial-mesenchymal transition, inflammation, oxidative stress, and metabolic rewiring. We further discuss emerging lncRNA signatures that reflect nutritional and metabolic states, their potential utility as biomarkers for individualized dietary interventions, and their integration into liquid biopsy platforms. Leveraging multi-omics datasets and systems biology, we outline AI-driven frameworks to map nutrient-lncRNA regulatory networks and identify tar-getable nodes for cancer chemoprevention. Finally, we address translational challenges, including compound bioavailability, inter-individual variability, and limited clinical validation, and propose future directions for incorporating lncRNA profiling into preci-sion nutrition-guided cancer prevention trials. Together, these insights position lncRNAs at the nexus of diet and cancer biology and establish a foundation for mechanistically informed precision nutrition strategies in cancer chemoprevention.

Autophagy plays a multifaceted role in cancer, acting as a tumor suppressor in early stages while promoting survival in advanced disease. In ovarian cancer, the regulatory landscape of autophagy, particularly the role of long non-coding RNAs (lncRNAs), remains poorly defined. Here, we identify the lncRNA ZFAS1 as a key modulator of autophagy under starvation-induced conditions in high-grade serous ovarian cancer (HGSOC). Transcriptomic and functional analyses reveal consistent upregulation of ZFAS1 during autophagy induction. Silencing ZFAS1 disrupts autophagic flux, leading to the accumulation of p62 and LC3, indicative of impaired autophagy clearance. Mechanistically, ZFAS1 suppresses miR302, thereby enhancing BNIP3L expression, a known mitophagy regulator that promotes mitochondrial clearance and survival un-der metabolic stress. Clinical dataset analyses confirm a significant correlation be-tween ZFAS1 overexpression, BNIP3L upregulation, and poor survival outcomes in ovarian cancer patients. While autophagy exerts tumor-suppressive effects in some in-stances, our data reveals a context-specific lncRNA-mediated mechanism by which autophagy supports tumor survival. These findings define a novel ZFAS1-miR302-BNIP3L axis and highlight ZFAS1 as a potential target for disrupting autophagy-dependent resistance in ovarian cancer.

Background/Objectives: Ovarian cancer is a leading cause of gynecological cancer mortality worldwide, often diagnosed at advanced stages due to vague symptoms and the lack of effective early detection methods. Long non-coding RNAs (lncRNAs) have emerged as key regulators in cancer biology, influencing cellular processes such as proliferation, apoptosis, and chemoresistance. This review explores the multifaceted roles of lncRNAs in ovarian cancer pathogenesis and their potential as biomarkers and therapeutic targets. Methods: A comprehensive literature review was conducted to analyze the structural and functional characteristics of lncRNAs and their contributions to ovarian cancer biology. This includes their regulatory mechanisms, interactions with signaling pathways, and implications for therapeutic resistance. Advanced bioinformatics and omics approaches were also evaluated for their potential in lncRNA research. Results: The review highlights the dual role of lncRNAs as oncogenes and tumor suppressors, modulating processes such as cell proliferation, invasion, and angiogenesis. Specific lncRNAs, such as HOTAIR and GAS5, demonstrate significant potential as diagnostic biomarkers and therapeutic targets. Emerging technologies, such as single-cell sequencing, provide valuable insights into the tumor microenvironment and the heterogeneity of lncRNA expression. Conclusions: LncRNAs hold transformative potential in advancing ovarian cancer diagnosis, prognosis, and treatment. Targeting lncRNAs or their associated pathways offers promising strategies to overcome therapy resistance and enhance personalized medicine. Continued research integrating omics and bioinformatics will be essential to unlock the full clinical potential of lncRNAs in ovarian cancer management.

Background/Objectives: Ovarian cancer is a leading cause of gynecological cancer mortality worldwide, often diagnosed at advanced stages due to vague symptoms and lack of effective early detection methods. Long non-coding RNAs (lncRNAs) have emerged as key regulators in cancer biology, influencing cellular processes such as proliferation, apoptosis, and chemoresistance. This review explores the multifaceted roles of lncRNAs in ovarian cancer pathogenesis and their potential as biomarkers and therapeutic targets. Methods: A comprehensive literature review was conducted to analyze the structural and functional characteristics of lncRNAs and their contributions to ovarian cancer biology. This includes their regulatory mechanisms, interactions with signaling pathways, and implications for therapeutic resistance. Advanced bioinformatics and omics approaches were also evaluated for their potential in lncRNA research. Results: The review highlights the dual role of lncRNAs as oncogenes and tumor sup-pressors, modulating processes such as cell proliferation, invasion, and angiogenesis. Specific lncRNAs, such as HOTAIR and GAS5, demonstrate significant potential as di-agnostic biomarkers and therapeutic targets. Emerging technologies, such as single-cell sequencing, provide valuable insights into the tumor microenvironment and the het-erogeneity of lncRNA expression. Conclusions: LncRNAs hold transformative potential in advancing ovarian cancer di-agnosis, prognosis, and treatment. Targeting lncRNAs or their associated pathways offers promising strategies to overcome therapy resistance and enhance personalized medicine. Continued research integrating omics and bioinformatics will be essential to unlock the full clinical potential of lncRNAs in ovarian cancer management.

Peritoneal cancers present significant clinical challenges with poor prognosis. Understanding the role of cancer cell metabolism and cancer-promoting metabolites in peritoneal cancers can provide new insights into the mechanisms that drive tumor progression and can identify novel therapeutic targets and biomarkers for early detection, prognosis, and treatment response. Cancer cells dynamically reprogram their metabolism to facilitate tumor growth and overcome metabolic stress, with cancer-promoting metabolites such as kynurenines, lactate, and sphingosine-1-phosphate promoting cell proliferation, angiogenesis, and immune evasion. Targeting cancer-promoting metabolites could also lead to the development of effective combinatorial and adjuvant therapies involving metabolic inhibitors for the treatment of peritoneal cancers. With the observed metabolomic heterogeneity in cancer patients, defining peritoneal cancer metabolome and cancer-promoting metabolites holds great promise for improving outcomes for patients with peritoneal tumors and advancing the field of precision cancer medicine. This review provides an overview of the metabolic signatures of peritoneal cancer cells, explores the role of cancer-promoting metabolites as potential therapeutic targets, and discusses the implications for advancing precision cancer medicine in peritoneal cancers.