Bcl-2-related ovarian killer (BOK) mRNA (BOK mRNA)

Bcl-2-related ovarian killer (BOK) is a pro-apoptotic member of the BCL-2 family, structurally and functionally similar to the apoptotic effectors BAX and BAK (1.2.1, 1.2.2). BOK mRNA encodes a protein that is constitutively active and primarily regulated through the endoplasmic reticulum-associated degradation (ERAD) pathway, which targets it for rapid proteasomal destruction under normal conditions (1.2.1). The BOK gene is frequently deleted or its mRNA expression is significantly downregulated in various human malignancies, including ovarian, non-small cell lung, and colorectal cancers, suggesting a critical role as a tumor suppressor (1.2.1, 1.2.5). BOK mRNA stability and translation are further modulated by microRNAs such as miR-296-5p and RNA-binding proteins like TRIM28, which can lead to its silencing in cancer cells (1.2.1). Targeting BOK mRNA via RNA-based modalities, such as antisense oligonucleotides (ASOs) or small interfering RNAs (siRNAs), represents a potential therapeutic strategy to restore apoptotic sensitivity in tumors or to modulate cell death in neurodegenerative and reproductive disorders (1.3.1, 1.3.2). Additionally, BOK is involved in non-apoptotic cellular processes, including the regulation of mitochondrial dynamics and calcium signaling through interactions with IP3 receptors (1.2.1, 1.2.2).

Other names

BCL2L9 mRNABOKL mRNAMatador mRNABcl-2-related ovarian killer transcript

RNA interference, Antisense inhibition