Bcl-2-like protein 10 (BCL2L10)

Bcl-2-like protein 10 (BCL2L10) is a member of the Bcl-2 protein family involved in the regulation of apoptosis, acting primarily as an **anti-apoptotic protein**. It contains BH4, BH1, and BH2 domains, and can hetero- or homodimerize with related proteins such as BCL2, BCL2L1 (Bcl-xL), and BAX[1][3][4]. BCL2L10 inhibits apoptosis mainly by preventing cytochrome c release from mitochondria and caspase activation[1][3]. It also regulates calcium signaling by interacting with the inositol 1,4,5-trisphosphate receptor, reducing calcium release from the endoplasmic reticulum[3]. In cancer, BCL2L10 promotes tumor cell migration, invasion, and vasculogenic mimicry, partially through upregulation and activation of MMP2, MMP9, uPAR, and ERK phosphorylation[2]. Overexpression in tumors like melanoma, gastric cancer, and leukemia, is associated with aggressive tumor features, poor prognosis, and chemoresistance[2][3]. As such, BCL2L10 is considered a **therapeutic target** in oncology, particularly in modulating anti-apoptotic pathways[2][3].

Other names

Bcl-BDIVABooBCLBAnti-apoptotic protein BooAnti-apoptotic protein NrHApoptosis regulator Bcl-Bdeath inducer binding to vBcl-2 and Apaf-1

Inhibition of anti-apoptotic BCL2L10 to sensitize cancer cells to apoptosis (e.g. by disrupting BCL2L10 function with inhibitors) Modulation of apoptosis by BCL2L10 overexpression (anti-apoptotic effect)