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Homo sapiens (human) FOXP4 antisense RNA 1 (FOXP4-AS1) URS00007E36F3_9606

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FOXP4-AS1: FOXP4-AS1 is a long non-coding RNA (lncRNA) that has been implicated in various cellular processes, including cell proliferation, migration, invasion, and apoptosis [PMC7094166] [PMC9592412] [PMC8973600]. It has been found to be upregulated in gastric cancer patients at late tumor stages and is associated with poorer overall survival [PMC7094166]. FOXP4-AS1 is also highly expressed in colorectal cancer (CRC) tissue and has been shown to promote cancer cell proliferation, inhibit apoptosis, and downregulate tumor-suppressor gene expression [PMC9202991]. In prostate cancer (PCa), FOXP4-AS1 regulates the growth of cancer cells by regulating the expression of miR-3184-5p and FOXP4 [PMC7923982] [PMC6572815]. Additionally, FOXP4-AS1 has been implicated in Ewing sarcoma cell lines A673 and SK-N-MC, where its subcellular localization was analyzed through a nuclear and cytoplasmic separation experiment [PMC8577041]. In hepatocellular carcinoma (HCC), the levels of FOXP4-AS1 were found to be associated with various clinical characteristics such as serum alpha-fetoprotein (AFP), serum aspartate aminotransferase (AST), size of tumor, liver cirrhosis, BCLC stage, and patient age [PMC6718253]. Furthermore, FOXP4-AS1 has been shown to sustain osteosarcoma cell growth by repressing LATS1 transcription through its interaction with LSD1 and EZH2 proteins [PMC6468368]. Overall, these studies highlight the diverse roles of FOXP4-AS1 in different types of cancers.

Genome locations

Gene Ontology annotations

Sequence

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CCCUGGUUUUCUGUGGAAAGUGAGCUUCUGGGUUCGACAGUGGGACCGGCACAGACCUUCCCGCAGCUACAGGCCAUACGACAACCCCGCUGCUCUUUCUUUCUGCGGGCACUCGGGCCAGUCCUAACAAUUGCCCCUCAAGCUGUGUGUGCUGCCCUAACCCUCAAUCCCGAACCCGAAACAGUGCGUGCUGGGACGAAUCUAGGCAGGUCUCCGAAACCGGGGUGAAGAUGCUGAAGUUCAGGUCAUUCCGGACUCCUGACGCCGCCAGUCCCGCGGUGAGACGUGAGCGCCAUUGGCGUCCGUGGCCUCUGUUUCCGUGGCAACCUAGUAACCAUUAAUUUUCAAUUAAAGGAGACAAAAAGCUCGAUGACAGCUCCAGGUCUGCUGAAGAUGUCAAGAAUCUGUAUUAAUAUACAGCAAGAGAGCAUAAUUGUGUGUCCAUCUUCCAGAGCAGCGAAAAAUGGAGGGAUAAUUACCAGCUCGAAAGCCACUCUGUAAUUUAGUUCUUACUGUCACCACAGCCCUACACAUUAGCAUAAAUUAAAAGCAGAGUUUAUUGUUAUCAAAGUGCAAAAAAAAAAAAAA

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Publications