{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n LINC01355 exhibits distinct functional roles in cancer that appear to be context‐dependent. In breast cancer, LINC01355 is significantly downregulated compared to non-malignant breast epithelial cells. Experimental overexpression of LINC01355 inhibited proliferation, colony formation, and tumorigenesis by arresting cancer cells in the G0/G1 phase. Mechanistically, LINC01355 interacts with and stabilizes the FOXO3 protein, which facilitates the transcriptional repression of CCND1; disruption of FOXO3 or forced CCND1 expression reverses these growth-suppressive effects."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Conversely, in oral squamous cell carcinoma (OSCC) LINC01355 is upregulated, and its knockdown significantly represses cell proliferation, migration, and invasion. In OSCC, reduced LINC01355 not only diminishes malignant behaviors but also promotes antitumor immunity by enhancing CD8+ T cell survival and cytolytic activity. These effects are mediated, at least in part, through the inactivation of the Notch signaling pathway, as evidenced by decreased levels of Notch-1, JAG-1, and HES-1; moreover, inhibition of Notch1 counteracts the oncogenic influence of LINC01355."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ""}]}, {"type": "t", "text": "\n \n "}, {"type": "p", "children": [{"type": "t", "text": "\n Collectively, these findings indicate that LINC01355 may serve as a tumor suppressor in breast cancer via FOXO3-mediated repression of cell cycle progression, while in OSCC it appears to promote tumorigenesis and suppress immune responses through modulation of the Notch pathway. The opposing roles of LINC01355 in different tumor types underscore the importance of cancer-specific context in determining its biological and potential therapeutic significance.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Bolun Ai, Xiangyi Kong, Xiangyu Wang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "LINC01355 suppresses breast cancer growth through FOXO3-mediated transcriptional repression of CCND1."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cell Death Dis (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41419-019-1741-8"}], "href": "https://doi.org/10.1038/s41419-019-1741-8"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31243265"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31243265"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Chen Zou, Siyuan Wu, Haigang Wei, et al. "}, {"type": "b", "children": [{"type": "t", "text": "LINC01355 Contributes to Malignant Phenotype of Oral Squamous Cell Carcinoma and Cytotoxic T Cell Infiltration via Activating Notch Signaling Pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Immunol Res (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1155/2021/1830790"}], "href": "https://doi.org/10.1155/2021/1830790"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "34355042"}], "href": "https://pubmed.ncbi.nlm.nih.gov/34355042"}]}]}]}