{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nOpa interacting protein 5 (OIP5) is emerging as an important protein with multifaceted roles in cell cycle regulation and tumorigenesis. Multiple studies have demonstrated that OIP5 is markedly overexpressed in a variety of human cancers—including colorectal, lung, esophageal, hepatocellular, breast, nasopharyngeal, oral, ovarian, and even certain glioblastomas—and its upregulation is significantly associated with poor prognosis, enhanced proliferation, and metastasis. Functionally, OIP5 overexpression is linked to altered cell cycle progression (for example, inducing multi‐septa formation and growth defects), while its suppression by RNA interference in cancer cell lines results in cell cycle arrest and apoptosis. Moreover, OIP5 has been classified as a cancer/testis antigen, and its stabilization (for instance, via interaction with proteins such as Raf1) appears to promote oncogenic signaling pathways such as AKT/mTOR and GSK‑3β/β‑catenin that are critical for tumor growth and metastasis; in specific contexts, such as in glioblastoma, OIP5 expression has even been correlated with an improved response to chemotherapeutic agents."}, {"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 addition to the protein‐coding transcript, the long non‐coding antisense RNA counterpart (lncRNA OIP5‑AS1) has been shown to execute complementary regulatory roles in both oncogenic and non‑malignant contexts. Acting as a competing endogenous RNA, OIP5‑AS1 modulates the expression of key effectors by sponging distinct microRNAs—including miR‑448, miR‑367‑3p, miR‑98‑5p, miR‑139‑5p, and miR‑34a—and thus influences pathways governing cell proliferation, migration, invasion, apoptosis, and resistance to radiotherapy or chemotherapy in cancers such as colorectal carcinoma, lung adenocarcinoma, gastric cancer, and glioma. Beyond its roles in cancer, OIP5‑AS1 has been implicated in a range of other pathophysiological processes, including the regulation of inflammatory responses in rheumatoid arthritis, modulation of endothelial cell injury and allergic responses, control of chondrocyte function in osteoarthritis, and even the promotion of trophoblast proliferation and migration via STAT3 signaling in the context of placental development."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Ho-Kyung Chun, Kyung-Sook Chung, Hee Cheol Kim, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Loss of the Opa interacting protein 5 inhibits breast cancer proliferation through miR-139-5p/NOTCH1 pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Gene (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.gene.2016.11.046"}], "href": "https://doi.org/10.1016/j.gene.2016.11.046"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "27916718"}], "href": "https://pubmed.ncbi.nlm.nih.gov/27916718"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Maryam Beigom Mobasheri, Reza Shirkoohi, Mohammad Hossein Modarressi "}, {"type": "b", "children": [{"type": "t", "text": "Cancer/Testis OIP5 and TAF7L Genes are Up-Regulated in Breast Cancer."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Asian Pac J Cancer Prev (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.7314/apjcp.2015.16.11.4623"}], "href": "https://doi.org/10.7314/apjcp.2015.16.11.4623"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26107214"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26107214"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Qihang Yan, Li Liu, Han Yang, et al. 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