Lycorine induces apoptosis of acute myeloid leukemia cells and inhibits triglyceride production via binding and targeting FABP5

Liang, Xinming; Fu, Wenli; Peng, YuHui; Duan, Jicheng; Zhang, Ting; Fan, Daogui; Wang, Hong; Qi, Xiaolan; Wu, ChangXue; He, Yan; Yu, Wei; Zhou, Jing; Guo, Pengxiang; Bai, Hua; Zhang, Qifang

doi:10.1007/s00277-023-05169-7

Cited by 4 publications

(4 citation statements)

References 39 publications

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“…Notably, research has demonstrated that lycorine effectively inhibits autophagy and exhibits robust anti-proliferative activity both in vivo and in vitro against multiple myeloma [ 18 ]. Furthermore, studies have unveiled lycorine's inhibitory effects on the proliferation of acute myeloid leukemia, B-cell acute lymphoblastic leukemia, and chronic lymphocytic leukemia cells [ 19 – 21 ]. Previous literature has reported that lycorine induces cell cycle arrest specifically in the G0/G1 phase of K562 cells [ 10 ].…”

Section: Discussionmentioning

confidence: 99%

Lycorine attenuated proliferation and induced apoptosis on imatinib-resistant K562 cell by inhibiting autophagy

Bai,

Feng,

Chen

et al. 2024

Discov Onc

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Background Tyrosine kinase inhibitor (TKI) resistance is a significant factor exacerbating the burden on chronic myeloid leukemia (CML) patients and impacting clinical efficacy. The main goal is to offer new insights into overcoming drug resistance in treating CML. Methods Imatinib (IM) resistant K562/IM cells were generated using gradient induction. Responses to IM, lycorine, and autophagy modulators were assessed using CCK-8. Protein expression of Beclin-1, Atg5, LC3, Caspase-3, P62, Bax, Bcl-2, and P-gp was detected using Western blot. Lycorine-induced apoptosis and cell cycle changes were evaluated through flow cytometry, while autophagy alterations were detected using monodansylcadaverine (MDC) staining. In the K562/IM mice model, non-obese diabetic severe combined immunodeficent (NOD-SCID) mice were subcutaneously inoculated with K562/IM cells. After 17 days of lycorine injection, assessments included tumor size, hematoxylin–eosin (HE) staining, and Ki67 expression. Results After 72 h of IM treatment, K562/IM cells showed a 55.86-fold increase in drug resistance compared to K562 cells. Lycorine treatment for 24 h inhibited cell proliferation and induced G0/G1 phase cell cycle arrest and apoptosis in both K562 and K562/IM cells. MDC staining indicated reduced autophagy in K562/IM cells, mitigated by lycorine. In vivo experiments demonstrated reduced tumor size and Ki67 proliferation index in the lycorine treatment group (K562+L, K562/IM+L) compared to the control group, particularly in the drug-resistant group. However, no significant change in Ki67 was observed in the K562 group after lycorine treatment. Conclusion In summary, K562/IM cells displayed heightened autophagy levels compared to K562 cells. Lycorine effectively impeded the proliferation of K562/IM cells through diverse mechanisms, including reduced autophagy, enhanced apoptosis, and induced cell cycle arrest.

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Section: Discussionmentioning

confidence: 99%

Lycorine attenuated proliferation and induced apoptosis on imatinib-resistant K562 cell by inhibiting autophagy

Bai,

Feng,

Chen

et al. 2024

Discov Onc

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“…Molecular docking revealed that lycorine interacts with FABP5 through Ile54, Thr56, Thr63, and Arg109 with an affinity of −9.13 kcal/ mol. 130 FABP7 and Other FABP Inhibitors. FABP7 is mainly expressed in microglia and astrocytes of the central nervous system and, like FABP3 and FABP5, participates in nociception.…”

Section: ■ Fabpsmentioning

confidence: 99%

“…Recently, Liang et al identified lycorine (compound 112 ) as an FABP5 inhibitor for treating acute myeloid leukemia (Figure ). Molecular docking revealed that lycorine interacts with FABP5 through Ile54, Thr56, Thr63, and Arg109 with an affinity of −9.13 kcal/mol …”

Section: Fabpsmentioning

confidence: 99%

Recent Advances on Small-Molecule Inhibitors of Lipocalin-like Proteins

Chen,

Pan,

Liu

et al. 2024

J. Med. Chem.

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Small-Molecule Inhibitors against RBPs. Synthetic retinoids utilize the ligand-binding characteristics of RBP4 as one type of small-molecule inhibitor. However, nonretinoid ligands can also serve as small-molecule RBP4 inhibitors. Both types of inhibitors target the lipocalin-domain of RBP4 and can therefore be classified into these two groups.Retinoids. N-(4-Hydroxyphenyl)retinamide (also known as fenretinide, Figure 2, compound 1) is a retinol analog that Figure 2. Chemical structures for reported RBP4 small-molecule inhibitors.

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“…Bioinformatics analysis revealed that upregulation of FABP5 expression facilitates acute myeloid leukemia (AML) cell viability, protects AML cells from apoptosis. LYC downregulated the expression levels of FABP5 and its target PPARγ, impaired AML cell viability, and triggered apoptosis ( Liang et al, 2023 ). By performing extracellular, cytoplasmic, and nuclear roles, HMGB1 is crucial for stress signaling as well as for the activation of autophagy.…”

Section: Natural Product—derived Compounds Overcome Cancer Drug Resis...mentioning

confidence: 99%

Natural products reverse cancer multidrug resistance

Zou,

Chen,

Luo

et al. 2024

Front. Pharmacol.

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Cancer stands as a prominent global cause of death. One of the key reasons why clinical tumor chemotherapy fails is multidrug resistance (MDR). In recent decades, accumulated studies have shown how Natural Product-Derived Compounds can reverse tumor MDR. Discovering novel potential modulators to reduce tumor MDR by Natural Product-Derived Compounds has become a popular research area across the globe. Numerous studies mainly focus on natural products including flavonoids, alkaloids, terpenoids, polyphenols and coumarins for their MDR modulatory activity. Natural products reverse MDR by regulating signaling pathways or the relevant expressed protein or gene. Here we perform a deep review of the previous achievements, recent advances in the development of natural products as a treatment for MDR. This review aims to provide some insights for the study of multidrug resistance of natural products.

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Lycorine induces apoptosis of acute myeloid leukemia cells and inhibits triglyceride production via binding and targeting FABP5

Cited by 4 publications

References 39 publications

Lycorine attenuated proliferation and induced apoptosis on imatinib-resistant K562 cell by inhibiting autophagy

Lycorine attenuated proliferation and induced apoptosis on imatinib-resistant K562 cell by inhibiting autophagy

Recent Advances on Small-Molecule Inhibitors of Lipocalin-like Proteins

Natural products reverse cancer multidrug resistance

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