For the first time in the world, a Korean research team discovered how cellular aging can spread systemically through the bloodstream—offering new insights and a potential therapeutic strategy to combat aging-related decline.

Professor Ok Hee Jeon's research group at the Department of Convergence Medicine, Korea University's College of Medicine, discovered that High Mobility Group Box 1 (HMGB1),a key extracellular senescence-associated secretory phenotype (SASP) factor, plays a critical role in transmitting senescence from aging cells to distant tissues.

Ovarian cancer (OC) remains the deadliest gynecologic malignancy, with platinum-based chemotherapies such as carboplatin serving as the standard first-line treatment. However, the emergence of carboplatin resistance presents a major therapeutic challenge, and the underlying mechanisms remain incompletely understood. In this study, Dr. Tao Lu’s group from Indiana University School of Medicine, employed a novel validation-based insertional mutagenesis (VBIM) technique to identify genes that confer resistance to carboplatin in human epithelial OC cells. This screen revealed hematological and neurological expressed 1-like (HN1L/JPT2) as a previously unrecognized contributor to drug resistance. HN1L overexpression enhanced resistance to carboplatin, whereas shRNA-mediated knockdown sensitized OC cells to treatment. Mechanistically, HN1L promoted resistance by activating nuclear factor κB (NF-κB) signaling. In addition, HN1L depletion reduced anchorage-independent growth in vitro and impaired tumorigenicity in a xenograft model of OC. Immunohistochemical (IHC) analysis demonstrated elevated HN1L expression in both OC cell lines and patient tissues across multiple disease stages. These findings identify HN1L as a novel carboplatin resistance gene and suggest that targeting HN1L may represent a promising strategy for overcoming platinum resistance in OC.