ArticleJournal of cellular and molecular medicine2025
LAPTM5 Confers the Resistance to Venetoclax via Promoting the Autophagosome-Lysosome Fusion in Multiple Myeloma.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- Targeting LAPTM5 enhances AML sensitivity to cytarabine through autophagy inhibition.Cell death & disease · 2026Article
- LAPTM proteins in neurological disorders - Autophagy-lysosome dysfunction and therapeutic targets: A review.Biomolecules & biomedicine · 2026Review
- Silencing of telomerase RNA component induces autophagy and ferroptosis in A549 and H838 lung cancer cells via AMPK-mediated signaling.Molecular and cellular biochemistry · 2026Article
- MAMDC2-AS1 Induces Cuproptosis in Relapsed and Refractory Multiple Myeloma.Cancer reports (Hoboken, N.J.) · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Multiple myeloma (MM) is a haematological lymphoid malignancy marked by significant morbidity due to severe complications. Despite advances in targeted therapies, including proteasome inhibitors and the BCL-2 inhibitor venetoclax, drug resistance frequently occurs, with the underlying mechanisms poorly understood. This study investigates the role of lysosome-associated protein transmembrane 5 (LAPTM5) in conferring resistance to venetoclax in relapsed MM. Using comprehensive analyses of publicly available databases and experimental validation, we demonstrated that LAPTM5 is upregulated and enhances autophagy in recurrent multiple myeloma cells, which is a key process for cell homeostasis and drug resistance. Mechanistic studies reveal that LAPTM5 facilitates autophagic flux, linking it to the cellular catabolic processes essential for survival under therapeutic stress. Our findings highlight the underexplored functions of LAPTM5 in modulating autophagy and drug resistance, we demonstrate that LAPTM5 confers resistance to venetoclax by enhancing autophagy, suggesting that targeting LAPTM5 may provide new avenues for overcoming treatment challenges. This research underscores the potential function of LAPTM5 as a therapeutic target in improving outcomes in MM treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.