{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTPX2 is a pivotal microtubule‐associated protein that orchestrates proper mitotic spindle assembly. It directly binds to and recruits Aurora A kinase to spindle microtubules, thereby promoting microtubule nucleation, stabilization and the formation of a robust bipolar spindle. In addition, TPX2 modulates the activity of motor proteins—such as Eg5—to ensure correct spindle pole separation and appropriate microtubule flux, which collectively determine spindle length and integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nTPX2 activity is tightly controlled during the cell cycle. It is subject to ubiquitin‐mediated degradation via the APC/C complex during mitotic exit, thereby ensuring its timely clearance once its spindle assembly functions are complete. Conversely, TPX2 binding activates and simultaneously protects Aurora A kinase from degradation—a balance further fine‐tuned by phosphatases (for example, PP6) and demarcated by detailed structural features revealed by cryo–electron microscopy analyses. These studies have provided novel insight into how TPX2 associates with microtubules and is regulated by the importin/Ran system."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its essential mitotic roles, aberrant TPX2 expression is increasingly recognized as a hallmark of numerous human cancers. Elevated TPX2 levels correlate with aggressive tumor phenotypes and poor patient prognosis in a diverse array of malignancies—including cervical, salivary, astrocytic, breast, lung, colorectal, hepatocellular, pancreatic, prostate, esophageal and malignant peripheral nerve sheath tumors. Dysregulated TPX2 contributes to enhanced cell proliferation, migration, invasion and apoptotic resistance. Its integration into complex regulatory networks is underscored by its modulation by non–coding RNAs (for example, circular RNAs and long non–coding RNAs that act via microRNAs and transcription factors such as E2F4 and GLIPR1) and by its interactions with additional spindle assembly regulators like RHAMM, as well as its involvement in DNA damage repair and replication fork stabilization. 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