CBR3 antisense RNA 1 (non-protein coding) (CBR3-AS1)

CBR3 antisense RNA 1 (CBR3-AS1), also known as PlncRNA-1, is a **long non-coding RNA (lncRNA)** initially identified as upregulated in prostate cancer[1][2][4][6]. It is transcribed antisense to the carbonyl reductase 3 (CBR3) gene and is overexpressed in multiple cancers, including prostate, colorectal, osteosarcoma, breast, and chronic myeloid leukemia[1][5]. Elevated CBR3-AS1 expression is linked to worse overall and disease-free survival, increased tumor size, lymph node involvement, metastasis, and higher TNM stage[1]. Functional studies demonstrate that CBR3-AS1 promotes tumor cell proliferation, migration, invasion, EMT, and chemoresistance—primarily through posttranscriptional regulation, sponging of microRNAs (such as those targeting the androgen receptor), and modulation of PTEN/AKT, TGF-β1, and androgen receptor (AR) pathways[2][3][4][6]. Silencing CBR3-AS1 inhibits cancer cell proliferation and promotes apoptosis, highlighting its potential as both a biomarker and therapeutic target in oncology settings[1][2][4][6]. Currently, there are no approved drugs that directly target CBR3-AS1; RNA interference-based experimental approaches are used in research models[1][2][5].

Other names

PlncRNA-1prostate cancer-up-regulated long noncoding RNA 1PlncRNA1

Silencing or knockdown of CBR3-AS1/PlncRNA-1 can suppress tumor cell proliferation, migration, invasion, and EMT, and promote apoptosis, likely via modulation of genes such as PTEN, components of the AKT pathway, TGF-β1, or androgen receptor signaling[2][3][4][6].