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Functional study of Esco2 in promoting proliferation and survival of acute myeloid leukemia cells

LI Pu-Jiao¹, YUAN Shi-Ru², SUN Guo-Huan², CHENG Hui^2,*

¹Haihe Laboratory of Cell Ecosystem, Tianjin Medical University, Tianjin 300070, China；²National Key Laboratory of Blood Science, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Institute of Hematology and Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China

Abstract

The present study aimed to investigate the expression pattern of Esco2 in acute myeloid leukemia (AML) and its role in regulating the biological behavior of AML cells. The expression level of ESCO2 and its association with prognosis in patients with AML were analyzed using the TCGA-LAML and GTEx datasets. An sgRNA-mediated Esco2 depletion model was established in MLL-AF9-driven AML cells, and its function was validated through both in vitro and in vivo experiments. A murine bone marrow transplantation model was used to evaluate the effects of Esco2 depletion on leukemia progression. Colony formation assay, cell proliferation assay, and Annexin V-based flow cytometry were performed to assess AML cell growth and apoptosis. Differential gene expression analysis and gene set enrichment analysis (GSEA) were conducted to explore Esco2-related pathways. The results showed that, compared with normal tissues, ESCO2 was significantly up-regulated in AML (P < 2.2 × 10-16), and high expression was significantly associated with poor prognosis (P = 0.04). Esco2 depletion markedly prolonged the survival of recipient mice (P = 0.0227) and reduced leukemic burden. In vitro experiments showed that Esco2 depletion suppressed proliferation and colony-forming capacity of AML cells and promoted apoptosis. Transcriptomic and Western blot analyses revealed that Esco2 depletion up-regulated the expression of E2F transcription factor 1 (E2F1) and cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) in AML cells, suggesting that Esco2 might be involved in cell cycle homeostasis and associated with cell cycle arrest and apoptosis. These results suggest that Esco2 is highly expressed in AML, whereas Esco2 depletion significantly suppresses leukemic cell proliferation and survival and delays AML progression, indicating its important biological significance in the occurrence and development of AML.

Key words: Esco2; acute myeloid leukemia (AML); cell proliferation; cell apoptosis

Received: 　　Accepted:

Corresponding author: 程辉　　E-mail:

DOI: 10.13294/j.aps.2026.0055

Citing This Article：

LI Pu-Jiao, YUAN Shi-Ru, SUN Guo-Huan, CHENG Hui. Functional study of Esco2 in promoting proliferation and survival of acute myeloid leukemia cells. Acta Physiol Sin 2026; 78 (4): 921-930 (in Chinese with English abstract).