{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have shown that TSGA10, originally defined as a cancer‐testis antigen, plays a multifaceted role in tumor biology. In various cancers, TSGA10 is differentially expressed and can act as a tumor suppressor by interacting with key hypoxia‐responsive factors, such as HIF‐1α and HIF‐2α, thereby disrupting their transcriptional activities. This in turn leads to reduced angiogenesis, invasion, and metastasis. In addition, several microRNAs (for example, miR-577, miR-23a, and miR-10b-3p) have been found to target TSGA10, modulating its levels and influencing cell cycle progression and tumor behavior under hypoxic conditions. Moreover, emerging evidence on distinct TSGA10 transcript variants with variable 5′ untranslated regions indicates the potential for fine-tuning its translation in the tumor microenvironment. These findings underscore the clinical potential of TSGA10 as a prognostic biomarker and therapeutic target in several malignancies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of immune regulation, TSGA10 has been identified as an autoantigen that may be targeted in autoimmune disorders. In patients with autoimmune polyendocrine syndrome type 1 (APS1) and, to a lesser extent, systemic lupus erythematosus (SLE), autoantibodies reactive to TSGA10 have been detected, suggesting its role as a target of aberrant immune responses. Moreover, its expression in antigen-presenting cells—where it interacts with cytoskeletal elements such as vimentin—hints at a potential role in modulating immune cell function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its implications in cancer and immune regulation, TSGA10 is critical for normal male reproductive function. It is abundantly expressed during spermatogenesis, and mutations or reduced expression of TSGA10 are associated with severe sperm defects, including acephalic spermatozoa and impaired spermatid differentiation. Disruptions in its function have been linked to altered autophagy and increased reactive oxygen species production, further implicating TSGA10 in the maintenance of sperm morphology and fertility."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ryo Tanaka, Toshiro Ono, Shuichiro Sato, et al. 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