{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPDZK1IP1, also known as MAP17, is a small, non‐glycosylated membrane‐associated protein whose aberrant expression and mutation have been documented in various tumor types. In malignant pleural mesotheliomas, for example, point mutations in PDZK1IP1 have been identified (5), while independent oncogene‐driven activation of its promoter has been reported in several carcinomas (2). Overexpression of PDZK1IP1/MAP17 enhances tumor cell survival by increasing reactive oxygen species (ROS) production and promoting resistance to apoptotic signals, as shown by its capacity to bypass tumor necrosis factor–induced growth arrest (1,3,4). In addition, its expression is up‐regulated in epidermal keratinocytes following cytokine exposure, suggesting a link with disrupted differentiation programs in inflammatory disease and cancer (6), and its elevated levels correlate with enhanced tumorigenic properties in breast and other cancers (7)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in promoting oxidative stress and survival, PDZK1IP1 directly modulates key oncogenic signaling pathways. It interacts with NUMB to sequester this negative regulator, thereby activating the Notch pathway and increasing the cancer stem cell–like population (13). In papillary thyroid cancer, PDZK1IP1 has been shown to accelerate cycloheximide‐induced degradation of p53—an effect counteracted by NUMB—highlighting its impact on tumor suppressor stability (24,25). Furthermore, PDZK1IP1 binds to Smad4, retaining it in the cytoplasm and consequently suppressing TGF‐β and BMP signaling pathways; this interference limits TGF‐β–induced cell growth inhibition and migration (18). Such interactions also contribute to the modulation of inflammatory responses within the tumor microenvironment, linking PDZK1IP1 to deregulated cell differentiation and survival cues (15)."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "12"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nClinically, abnormal PDZK1IP1/MAP17 expression serves as both a prognostic biomarker and a potential predictor of therapeutic response. Elevated PDZK1IP1 levels have been associated with improved outcomes following oxidative stress–inducing treatments in cervical tumors (8) and greater sensitivity to proteasome inhibition, as observed in sarcomas (10,12). Its overexpression correlates with aggressive tumor behavior in laryngeal carcinomas (9), intrahepatic cholangiocarcinoma (11), lung tumors (16), and hepatocellular carcinoma (22), while it also contributes to the maintenance of cancer stem cells in breast cancer (19) and is linked to colorectal cancer recurrence (23). In renal physiology, PDZK1IP1 acts as an accessory subunit for the Na⁺‐glucose cotransporter SGLT2, underscoring its diverse roles in both metabolic regulation and stress response (14,17). Moreover, insights into its mechanistic roles in non–small cell lung cancer (21) and associations with DNA damage responses as marked by H2AX phosphorylation (20) provide promising avenues for targeted therapies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "25"}]}, {"type": "t", "text": ""}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "M V Guijarro, M E Castro, L Romero, et al. 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