{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nStudies in monocytic cells have revealed that PBOV1 functions downstream of regulatory noncoding RNAs. In THP‐1 cells, the long noncoding RNA NTT—whose expression is driven by the transcription factor C/EBPβ—binds near the PBOV1 promoter via hnRNP‐U to upregulate PBOV1 expression. Overexpression of PBOV1 in these cells induced G1 cell cycle arrest, promoted differentiation into macrophages, and enhanced inflammatory cytokine (IL‑10 and CXCL10) and costimulatory molecule expression; notably, activation of the C/EBPβ/NTT/PBOV1 axis was evident in mononuclear cells from early rheumatoid arthritis patients, correlating with disease activity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nEvolutionary analyses have demonstrated that PBOV1 is a human‐specific, de novo–originated gene, absent from non‐primate genomes. Expressed in a broad array of tumor types but undetectable in normal adult or fetal tissues, PBOV1 transcription is driven by a GC‐poor, TATA‐box–containing promoter and may be modulated by pathways such as Hedgehog signaling. Intriguingly, high PBOV1 expression levels in cancers such as breast cancer and glioma have been associated with favorable clinical outcomes and decreased recurrence, suggesting that its expression might confer a selective disadvantage to cancer cells in certain contexts."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nIn ovarian cancer, PBOV1 appears to function as a tumor suppressor. Elevated levels of PBOV1 mRNA and protein in ovarian cancer cell lines and primary tumors were linked to lower histological grades, earlier pT/pN/pM stages, and improved overall survival. Functional studies further revealed that overexpression of PBOV1 inhibited cell proliferation and tumorigenesis in vitro and in animal models, underscoring its potential role in restraining ovarian cancer progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "3"}]}, {"type": "t", "text": ""}, {"type": "p", "children": [{"type": "t", "text": "\nConversely, in nasopharyngeal carcinoma (NPC) the PBOV1 oncogenic role is facilitated by complex interactions with noncoding RNAs. The lncRNA FBXL19‑AS1 was found to accelerate NPC progression by sponging microRNA‑431, a negative regulator of PBOV1. This post‑transcriptional de-repression of PBOV1 enhanced NPC cell viability, migration, and invasion, thus implicating the FBXL19‑AS1/miR‑431/PBOV1 axis as a potential therapeutic target in NPC."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}]}]}]}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Chin-An Yang, Ju-Pi Li, Ju-Chen Yen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "lncRNA NTT/PBOV1 Axis Promotes Monocyte Differentiation and Is Elevated in Rheumatoid Arthritis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Mol Sci (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3390/ijms19092806"}], "href": "https://doi.org/10.3390/ijms19092806"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30231487"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30231487"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Nikolay Samusik, Larisa Krukovskaya, Irina Meln, et al. "}, {"type": "b", "children": [{"type": "t", "text": "PBOV1 is a human de novo gene with tumor-specific expression that is associated with a positive clinical outcome of cancer."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "PLoS One (2013)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1371/journal.pone.0056162"}], "href": "https://doi.org/10.1371/journal.pone.0056162"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "23418531"}], "href": "https://pubmed.ncbi.nlm.nih.gov/23418531"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Lan Wang, Chun-Hao Niu, Shu Wu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "PBOV1 correlates with progression of ovarian cancer and inhibits proliferation of ovarian cancer cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Oncol Rep (2016)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3892/or.2015.4396"}], "href": "https://doi.org/10.3892/or.2015.4396"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "26549570"}], "href": "https://pubmed.ncbi.nlm.nih.gov/26549570"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Hongjun Dong, Chao Huang, Jingjing Huang "}, {"type": "b", "children": [{"type": "t", "text": "FBXL19‑AS1 promotes the progression of nasopharyngeal carcinoma by acting as a competing endogenous RNA to sponge miR‑431 and upregulate PBOV1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Med Rep (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.3892/mmr.2021.12286"}], "href": "https://doi.org/10.3892/mmr.2021.12286"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34278444"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34278444"}]}]}]}