본문으로 건너뛰기
← 뒤로

Dual-targeting Bcl-2-mediated apoptosis and synergistic pathways: Combinatorial strategies to overcome therapeutic resistance in cancer.

2/5 보강
Biochemical pharmacology 2026 Vol.247() p. 117802 Cell death mechanisms and regulation
TL;DR Breast cancer in Cotonou predominantly affects relatively young women and is often diagnosed at advanced stages, contributing to poor survival outcomes compared with high-income countries and strengthening early detection and prevention strategies should be a public health priority.
Retraction 확인
출처
PubMed DOI OpenAlex Semantic 마지막 보강 2026-04-29
OpenAlex 토픽 · Cell death mechanisms and regulation Autophagy in Disease and Therapy Phagocytosis and Immune Regulation

Cheng J, Wang H, Zhang Y, Liu G

📝 환자 설명용 한 줄

Breast cancer in Cotonou predominantly affects relatively young women and is often diagnosed at advanced stages, contributing to poor survival outcomes compared with high-income countries and strength

이 논문을 인용하기

BibTeX ↓ RIS ↓
APA Jiongjia Cheng, Haiying Wang, et al. (2026). Dual-targeting Bcl-2-mediated apoptosis and synergistic pathways: Combinatorial strategies to overcome therapeutic resistance in cancer.. Biochemical pharmacology, 247, 117802. https://doi.org/10.1016/j.bcp.2026.117802
MLA Jiongjia Cheng, et al.. "Dual-targeting Bcl-2-mediated apoptosis and synergistic pathways: Combinatorial strategies to overcome therapeutic resistance in cancer.." Biochemical pharmacology, vol. 247, 2026, pp. 117802.
PMID 41687827

Abstract

Dysregulation of apoptosis pathways is a defining characteristic of cancer, that has established pro-apoptotic activation as a fundamental therapeutic strategy in oncology. The B-cell lymphoma-2 (Bcl-2) family proteins serves as master regulators of mitochondrial apoptosis, with anti-apoptotic members constituting critical checkpoints in cancer cell survival. Across diverse cancer types, overexpression of anti-apoptotic Bcl-2 proteins is a universal mechanism driving cancer cells to evade apoptosis and acquire resistance to chemotherapy. However, relying solely on agents that induce the downregulation of anti-apoptotic Bcl-2 proteins has proven inefficient for cancer treatment. Notably, the observed synergy between Bcl-2 inhibitors and other anti-tumor agents supports the development of dual-targeting regimens as promising therapeutic approaches. Here, we comprehensively review the recent progress in dual-targeted apoptotic modulation, focusing on strategies that concurrently inhibit anti-apoptotic Bcl-2 family proteins and synergistic pathways. Emerging evidence demonstrates that Bcl-2/B cell lymphoma extra large (Bcl-xL)/myeloid cell leukemia 1 (Mcl-1) inhibitors (e.g., venetoclax and the derivatives) combined with p53/murine double minute 2 (MDM2) disruptors, epigenetic modifiers (e.g., histone deacetylase inhibitors), autophagy modulators, or kinases inhibitors, achieve synergistic potency. These rationally designed combination therapies effectively suppress compensatory upregulation of alternative anti-apoptotic proteins, overcome Bcl-2/Bcl-xL/Mcl-1-driven resistance and restore drug efficacy in apoptosis-deficient cancer subtypes. This paradigm shift offers substantial potential to advance precision oncology by establishing durable responses through simultaneous blockade of multiple survival axes, and carries tremendous promise in the next-generation evolution of cancer therapeutics.

MeSH Terms

Humans; Apoptosis; Neoplasms; Drug Resistance, Neoplasm; Proto-Oncogene Proteins c-bcl-2; Antineoplastic Agents; Animals; Drug Synergism; Antineoplastic Combined Chemotherapy Protocols; Signal Transduction

같은 제1저자의 인용 많은 논문 (5)