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Homo sapiens (human) ST8SIA6 antisense RNA 1 (ST8SIA6-AS1) URS000075A563_9606

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ST8SIA6-AS1: ST8SIA6-AS1 is a long non-coding RNA (lncRNA) that has been implicated in various types of cancer, including hepatocellular carcinoma (HCC), colorectal cancer, and breast cancer [PMC8139734] [PMC7288512] [PMC9837176]. In HCC, the expression of ST8SIA6-AS1 is upregulated in both tissues and cell lines [PMC8139734]. Silencing ST8SIA6-AS1 has been shown to inhibit cell viability, migration, and invasion in HCC cells, while promoting apoptosis through the miR-5195-3p/HOXB6 axis [PMC8139734]. In colorectal cancer cells, knockdown of ST8SIA6-AS1 reduces cell growth, migration, and invasion via the miR-5195/PCBP2 axis [PMC8139734]. Conversely, overexpression of ST8SIA6-AS1 in breast cancer cells enhances proliferation, invasion, and migration by activating the p38 MAPK signaling pathway [PMC7709816]. In HCC cell lines HCCLM3 and Huh7, silencing ST8SIA6-AS1 inhibits cell growth while promoting apoptosis [PMC9837176]. Furthermore, it has been suggested that ST8SIA6-AS1 may be involved in a ceRNA network in HCC [PMC7709816]. Knockout of ST8SIA6-AS1 leads to upregulation of E-cadherin expression and downregulation of vimentin expression in tumor tissues from nude mice with HCC xenografts [PMC9242794]. Overall, these findings highlight the potential role of ST8SIA6-AS1 as a regulator of tumor progression and suggest its potential as a therapeutic target for various types of cancer.

Genome locations

Gene Ontology annotations

Sequence

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GAGAAGGGAGGAGUUAUUCAGGCCUCCGCCAGCUUCUAGGCCCUGGGGAUGGUCUUUCACCUCCCUCUUUCUGAUCUCUUUUUCAUGCUCCUCCUUGCUCCAAAGAAAAGCCGGAUGGCAAAAGAGCCCAGAACCUAUUGGAACUGACAAAAUCAAGUCACGGCGCCUACAAAGAUGAGGGGCAGAUUCUGGCUGCCUUUUAAUUUCGUCCUUCACCUGAUAUCUGUGCCAGAGAAUGAUAAAAAUCAUAAUAAAGGAAAUAAUGGAAGAGGAGACUUAUGUUACUGGGGACAUCUAACAUAAUUAUUUUCCUGAUUCAGUGGCAUGGUUCAGUCUUCCAGGAGUUCUGCUACAGAGAAGAGAGUAACCCCCAUCCAUCAUGGCCAAAGCACCCAGUCAGGCUCCGCUCUGGAUCCAGCCCGACAAAUGCAACCCUUGAAUAGGGUUUGUGCAAGCAAACUGGAUGACGACCGAAGAAACCCUGUCGCUUCUGAGAAGACACCCAAUCCAAGAAUGUGAGUUCUGGAAAUGUCAUUAAAUGUCAGUUAUAUACAUGCAAAAAAAAAAAAAAAAA

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Publications