ANAPC11

ANAPC11 Full Name

anaphase promoting complex subunit 11

ANAPC11 Introduction

ANAPC11 (anaphase-promoting complex subunit 11) is a core catalytic component of the anaphase-promoting complex/cyclosome (APC/C), a multi-subunit Cullin-RING E3 ubiquitin ligase that controls one of the most clinically critical biological processes: cell-cycle progression. For researchers and clinicians facing uncontrolled proliferation in cancer or developmental dysregulation, ANAPC11 is increasingly recognized as a molecular "switch" that determines whether cells proceed through mitosis or are arrested for degradation of key regulatory proteins. Functionally, ANAPC11 cooperates with APC2 to form the catalytic center of APC/C, enabling ubiquitin transfer to substrates that govern metaphase-to-anaphase transition and mitotic exit, thereby ensuring genomic stability and orderly cell division.

Beyond its canonical role in mitosis, emerging evidence highlights ANAPC11 as a context-dependent regulator of differentiation, tissue growth, and protein stability networks that directly influence disease outcomes. In glioblastoma, single-cell transcriptomic analyses demonstrated that ANAPC11 acts as a fate-determining regulator of neuronal differentiation, where its high expression maintains proliferative tumor states while its knockdown induces cell-cycle exit and promotes neuron-like differentiation, significantly reducing tumor burden and extending survival in vivo. In parallel, plant developmental studies suggest APC11 is essential for organ size control via modulation of APC/C activity in meristematic regions, linking this subunit to fundamental growth regulation mechanisms across species. These findings collectively underscore ANAPC11 as more than a mitotic scaffold protein—it is a central regulator of growth decisions at the cellular and organismal level.

Clinically, dysregulation of ANAPC11 is increasingly associated with aggressive tumor phenotypes, metastasis, and therapy resistance, making it a high-value target for precision oncology strategies. In urothelial bladder cancer, ANAPC11 overexpression promotes FOXO3 ubiquitination and degradation, suppressing tumor-suppressive signaling and enhancing proliferation and lymph node metastasis, with strong correlations to poor patient prognosis. In breast cancer models, impaired APC/C function contributes to chemoresistance, while pharmacological activation of APC restores mitotic progression and resensitizes resistant cells to chemotherapeutics. Together, these studies highlight a pressing clinical challenge: ANAPC11-driven APC/C imbalance not only fuels tumor progression but also undermines treatment efficacy, positioning this subunit as a promising biomarker and therapeutic entry point for overcoming drug resistance and improving cancer outcomes.

Alternate Names for ANAPC11

ANAPC11; anaphase promoting complex subunit 11; APC11; Apc11p; HSPC214; anaphase-promoting complex subunit 11; cyclosome subunit 11; APC11 anaphase promoting complex subunit 11 homolog; hepatocellular carcinoma-associated RING finger protein; anaphase promoting complex subunit 11 (yeast APC11 homolog)

• 1.Yang R, et al.; Single-cell analyses identify anaphase-promoting complex subunit 11 as a switch controlling neuronal differentiation of glioblastoma cells. Genes Dis. 2023, 10(5):1802-1805.
  2.Yan D, et al.; The APC/C E3 ligase subunit ANAPC11 mediates FOXO3 protein degradation to promote cell proliferation and lymph node metastasis in urothelial bladder cancer. Cell Death Dis. 2023, 14(8):516.