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Cyclin-dependent kinase 6 antisense RNA 1 (CDK6-AS1), also known as BALR-2 (B-ALL associated long RNA-2), is a long non-coding RNA that acts as an enhancer RNA regulating expression of the adjacent CDK6 gene[1][3][6]. It is differentially overexpressed in various cancers, particularly B-cell acute lymphoblastic leukemia (B-ALL) and gastric cancer, and is associated with poor prognosis and chemoresistance, especially to glucocorticoids in B-ALL[1][2][6]. Mechanistically, CDK6-AS1 modulates cell cycle progression and proliferation, largely via regulating CDK6 and related gene expression. It is also implicated in the tumor microenvironment by reducing antitumor immune infiltration when highly expressed[1]. CDK6-AS1 is primarily studied as a prognostic and predictive biomarker rather than a classical drug target, but its functional impact on drug resistance and cancer progression makes it a focus of ongoing biomarker and lncRNA-targeted therapy research[1][2][6].
CDK6-AS1 does not act directly as a classic drug target. However, its biological mechanisms, which could be relevant for therapies impacting its pathway, include modulation of cell proliferation and survival by altering CDK6 and cell cycle gene expression, induction of chemoresistance by upregulation (e.g., increased glucocorticoid resistance via upregulated BALR-2/CDK6-AS1), and altered immune cell infiltration and tumor microenvironment.
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