ArticleGenes & diseases2026
SERHL regulates invasion and metastasis through KLF16-PLCB1/PRKCA signaling in gastric cancer cells.
Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Human SERHL, a pseudogene-derived lncRNA, plays a key role in cancer progression. However, the mechanism by which SERHL modulates gastric cancer (GC) is mostly unknown. This study found that SERHL was down-regulated in GC and inversely related to its malignancy. Overexpression of SERHL inhibited cell growth and metastasis in GC cells. Mechanistically, SERHL interacts with KLF16, promoting the degradation of KLF16 via ubiquitination in GC cells. The transcription factor KLF16 binds to the promoters of PLCB1 and PRKCA genes, increasing their expression and enhancing GC invasion and metastasis. SERHL reduces motility by inhibiting the KLF16-PLCB1/PRKCA signaling pathway in GC cells. These results highlight the function and mechanism of SERHL in GC progression, indicating that SERHL has the potential to be a diagnostic marker and therapeutic target in GC.
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