ArticleCancer medicine2020
Bcl-2/Bcl-xl inhibitor APG-1252-M1 is a promising therapeutic strategy for gastric carcinoma.
Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- B-Cell Lymphoma-Extra Large Promotes Gastric Tumorigenesis via Apoptosis-Independent Wnt-β-Catenin Activation and Peroxisome Proliferator-Activated Receptor γ Suppression.Cellular and molecular gastroenterology and hepatology · 2026Article
- BCL-2/BCL-xL inhibitor pelcitoclax with osimertinib forJournal for immunotherapy of cancer · 2026Article
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- The use of venetoclax in the treatment of acute lymphoblastic leukemia-a systematic review.Therapeutic advances in medical oncology · 2026Review
- The novel BCL-2/BCL-XL inhibitor APG-1252-mediated cleavage of GSDME enhances the antitumor efficacy of HER2-targeted therapy in HER2-positive gastric cancer.Acta pharmacologica Sinica · 2025Article
- The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
- Both direct and indirect suppression of MCL1 synergizes with BCLXL inhibition in preclinical models of gastric cancer.Cell death & disease · 2025Article
- Targeting Bcl-2 with Indole Scaffolds: Emerging Drug Design Strategies for Cancer Treatment.Mini reviews in medicinal chemistry · 2025Review
- Venetoclax therapy and emerging resistance mechanisms in acute myeloid leukaemia.Cell death & disease · 2024Review
- Review
- Mcl-1 levels critically impact the sensitivities of human colorectal cancer cells to APG-1252-M1, a novel Bcl-2/Bcl-XNeoplasia (New York, N.Y.) · 2022Article
- Strategies to Reduce the On-Target Platelet Toxicity of Bcl-xChembiochem : a European journal of chemical biology · 2022Review
- Protein-protein interactions between RUNX3 and ZEB1 in chronic lung injury induced by methamphetamine abuse.Frontiers in pharmacology · 2022Article
- Targeting the BCL-2-regulated apoptotic pathway for the treatment of solid cancers.Biochemical Society transactions · 2021Review
- Discovery, development and application of drugs targeting BCL-2 pro-survival proteins in cancer.Biochemical Society transactions · 2021Review
- CircGSK3B promotes RORA expression and suppresses gastric cancer progression through the prevention of EZH2 trans-inhibition.Journal of experimental & clinical cancer research : CR · 2021Article
- Gemcitabine and APG-1252, a novel small molecule inhibitor of BCL-2/BCL-XL, display a synergistic antitumor effect in nasopharyngeal carcinoma through the JAK-2/STAT3/MCL-1 signaling pathway.Cell death & disease · 2021Article
- Programmed cell death, redox imbalance, and cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2021Review
- Aberrant Bcl-x splicing in cancer: from molecular mechanism to therapeutic modulation.Journal of experimental & clinical cancer research : CR · 2021Review
- Therapeutics Targeting the Core Apoptotic Machinery.Cancers · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric carcinoma is the third major cause of cancer-related death in China. Bcl-2 and other BH3 family proteins are critically important in the process of apoptosis pathway, which may be a promising target. APG-1252-M1 specifically connects to Bcl-2 and Bcl-xl. The antitumor effect of APG-1252-M1 in six gastric cancer cells was identified by the Cell Counting Kit-8 assay. The expression level of proapoptotic proteins was evaluated by Western blot. Meanwhile, the cell cycle and apoptosis distributions were analyzed by flow cytometry and JC-1. Xenograft models were used to investigate the roles of APG-1252-M1 in suppressing the growth of tumors and enhancing the chemotherapy antitumor effect. The antitumor effect of APG-1252-M1 was time- and dose-dependent and acted by initiating apoptosis. The change of cell cycle distribution was not discovered in gastric cancer cells treated with APG-1252-M1. APG-1252-M1 also exhibited synergy with chemotherapy in vivo. The combined group inhibited xenograft tumor growth more obviously than the other groups. Moreover, Ki-67 was remarkably decreased in the combination group compared to other groups. In conclusion, APG-1252-M1 had a strong antitumor effect by inducing apoptosis and was synergistic with chemotherapy.
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