| Name | long intergenic non-protein coding RNA 1450 |
| Summary |
{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nA review of the provided abstracts reveals that members of the miR‐221/222 family are repeatedly implicated as key regulators of diverse cellular processes—including cell cycle progression, proliferation, apoptosis, differentiation, and inflammatory responses—in contexts ranging from cancer and cardiovascular disease to neural and immune functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "14"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNotably, while each abstract robustly characterizes miR‐221/222 functions—in regulating cell adhesion, migration, immune cell activation, tissue remodeling, and organ regeneration—none of the studies provide a direct evaluation of LINC01450. However, several reports in the list also explore long non‐coding RNAs (for example, lincRNA p21 in a neuronal context and lncRNA TUG1 in acute lung injury), and such molecules are increasingly recognized for their ability to “sponge” microRNAs, thereby modulating their availability and downstream activity. In light of this paradigm, it is plausible to propose that LINC01450 may serve a similar function by interacting with the miR‐221/222 cluster, ultimately influencing the expression of pivotal targets like cell cycle regulators (e.g. p27), pro‐apoptotic mediators, and inflammation‐related proteins"}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "27"}]}, {"type": "t", "text": ".\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nThus, by extrapolating from the extensive evidence linking miR‐221/222 to key regulatory networks across a broad spectrum of disease models—including oncogenesis, tissue repair, vascular remodeling, immune modulation, and even neuronal preservation—it is reasonable to hypothesize that LINC01450, as a long intergenic non‑coding RNA, might function as a competitive endogenous RNA (ceRNA) that sequesters miR‐221/222. Such an interaction could fine‑tune the abundance and activity of these microRNAs and, in turn, modulate the expression of targets such as p27, SIRT1, Foxp1, and others. This molecular interplay may influence critical processes like tumor progression, inflammatory cascades, and regenerative responses. Future studies are warranted to directly interrogate LINC01450’s role and validate its potential as an upstream modulator of miR‐221/222‐driven pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "43"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Beatrice Cardinali, Loriana Castellani, Pasquale Fasanaro, et al. 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| NCBI Gene ID | 101928744 |
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| Predicted Functions |
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| Co-expressed Genes |
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| Expression in Tissues and Cell Lines |
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LINC01450 has 0 functional associations with biological entities spanning 0 categories () extracted from 0 datasets.
Click the + buttons to view associations for LINC01450 from the datasets below.
If available, associations are ranked by standardized value
| Dataset | Summary |
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