{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nVMP1 is a central regulator of autophagy and organelle dynamics in mammalian cells. Multiple studies have shown that its expression initiates autophagosome formation by promoting the recruitment of key autophagic factors, including LC3 and Beclin 1, and activating the Class III phosphatidylinositol-3 kinase complex. In addition, VMP1 plays a critical role in the early steps of selective autophagy in specialized contexts—such as zymophagy in pancreatic acinar cells—where it helps sequester activated zymogen granules to protect against cell injury. Its localization at the endoplasmic reticulum, where it regulates contact sites with isolation membranes and other organelles via activity modulation of ER-resident proteins like SERCA, further underlines its importance in maintaining intracellular membrane homeostasis. These molecular actions are conserved across species and are further modulated by post-translational modifications such as ubiquitination, underscoring VMP1’s multifaceted role in orchestrating both bulk and selective autophagy."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer, VMP1 exhibits a dual behavior that appears to depend on the tumor type and cellular environment. In several malignancies—including pancreatic, breast, hepatocellular, colorectal, non‐small cell lung cancer, and even glioma—aberrant VMP1 expression has been linked both to enhanced oncogene‐induced autophagy that supports tumor cell survival and to alterations in cell–cell adhesion that modulate invasiveness and metastatic potential. For instance, oncogenic signals from KRAS and microRNAs (such as miR‑210 and miR‑21) regulate VMP1 expression, thereby impacting autophagic flux, cell proliferation, and invasion. In some cases, genomic rearrangements lead to fusion transcripts involving VMP1 that further associate with aggressive disease phenotypes. These multifaceted roles of VMP1 underscore its potential as both a prognostic marker and a therapeutic target in cancers."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical roles in autophagy and tumor biology, VMP1 is increasingly recognized as a key player in broader cellular stress responses and inter-organellar communication. Its functions extend to the maintenance of neuronal homeostasis, as evidenced by studies linking its deficiency to dopaminergic neurodegeneration, and to the regulation of host cell membrane remodeling during viral infections such as SARS‑CoV‑2, where loss of VMP1 disrupts double-membrane vesicle formation. Further, VMP1 is subject to intricate regulatory loops involving microRNAs and is modulated by lipid modifications that may influence extracellular vesicle secretion. Together, these emerging insights highlight the versatility of VMP1 as an integrator of membrane dynamics, stress adaptation, and intercellular communication in both health and disease."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Alejandro Ropolo, Daniel Grasso, Romina Pardo, et al. 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