BCL2L11, also known as BIM (Bcl-2-like protein 11), is a pro-apoptotic member of the BCL2 family. It plays a crucial role in regulating apoptosis, a programmed cell-death process, which is vital for maintaining tissue homeostasis, development, and immunity. Dysregulation of apoptosis is associated with various diseases [3].

In papillary thyroid cancer (PTC), BCL2L11 expression levels are reduced, and this reduction is correlated with TNM stage and lymph node metastasis. Silencing BCL2L11 can induce PTC cell activities, indicating its potential role in inhibiting cancer cell growth [1]. In childhood acute lymphoblastic leukemia, BCL2L11 polymorphisms are associated with corticosteroid-related osteonecrosis, influencing the viability of dexamethasone-treated lymphoblastoid cell lines [2]. In multiple myeloma, down-regulation of BCL2L11 by bone marrow stromal cells contributes to cell adhesion-mediated drug resistance, and up-regulation of BCL2L11 promotes apoptosis of myeloma cells [4]. In advanced NSCLC patients treated with osimertinib, germline BCL2L11 deletion polymorphism (BIM-del) is associated with poor clinical responses and outcomes, serving as a negative predictive and prognostic biomarker [5].

In conclusion, BCL2L11 is essential in apoptosis regulation. Studies, including those on gene polymorphisms and deletion polymorphisms, have revealed its significance in diseases such as papillary thyroid cancer, childhood acute lymphoblastic leukemia, multiple myeloma, and NSCLC. Understanding BCL2L11's function in these disease contexts may provide insights for developing novel therapeutic strategies.

References:

1. Shen, Yi, Li, Xiaoen, Xie, Rongli, Liu, Yaping, Ma, He. 2023. Expression Levels of MicroRNA-300/BCL2L11 in Papillary Thyroid Cancer and Their Clinical Diagnostic Values. In European surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes, 64, 342-351. doi:10.1159/000530682. https://pubmed.ncbi.nlm.nih.gov/37231813/

2. Plesa, Maria, Gagné, Vincent, Glisovic, Sanja, Sinnett, Daniel, Krajinovic, Maja. 2017. Influence of BCL2L11 polymorphism on osteonecrosis during treatment of childhood acute lymphoblastic leukemia. In The pharmacogenomics journal, 19, 33-41. doi:10.1038/s41397-017-0002-4. https://pubmed.ncbi.nlm.nih.gov/29282361/

3. Dai, Yun, Grant, Steven. . BCL2L11/Bim as a dual-agent regulating autophagy and apoptosis in drug resistance. In Autophagy, 11, 416-8. doi:10.1080/15548627.2014.998892. https://pubmed.ncbi.nlm.nih.gov/25700997/

4. Xie, Lingling, Wei, Jinhong, Gao, Zhihua, Ju, Shaoqing, Wang, Xudong. 2022. Significance of a tumor microenvironment-mediated P65-miR-30a-5p-BCL2L11 amplification loop in multiple myeloma. In Experimental cell research, 415, 113113. doi:10.1016/j.yexcr.2022.113113. https://pubmed.ncbi.nlm.nih.gov/35339472/

5. Li, Xuanzong, Zhang, Dai, Li, Butuo, Yu, Jinming, Wang, Linlin. 2020. Clinical implications of germline BCL2L11 deletion polymorphism in pretreated advanced NSCLC patients with osimertinib therapy. In Lung cancer (Amsterdam, Netherlands), 151, 39-43. doi:10.1016/j.lungcan.2020.12.002. https://pubmed.ncbi.nlm.nih.gov/33296806/