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September 18, 2025Open Access

TRPML1 signaling at lysosomes-mitochondria nexus drives triple-negative breast cancer mitophagy, metabolic reprogramming and chemoresistance

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Authors

ASAlia Kazim Rizvi SyedaSAShekoufeh AlmasiCBCory J. Benson

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Overview

Observational analysis reveals TRPML1 as a master regulator of mitophagy and metabolism in triple-negative breast cancer, suggesting potential therapeutic targets.

Key Points

  • TRPML1 knockdown impairs mitochondrial function and reprograms metabolism in triple-negative breast cancer cells, enhancing their sensitivity to treatment.
  • Lysosomal dysfunction due to TRPML1 loss contributes to mitochondrial fragmentation and alters inter-organelle communication in TNBC cells.
  • ML1-KD TNBC cells exhibit increased mitochondria-ER contact, which hinders autophagic flux and reduces oxidative defense mechanisms.
  • Targeting TRPML1 may offer a novel therapeutic strategy to exploit the metabolic vulnerabilities inherent in triple-negative breast cancer.

Cite This Study

Syeda et al. (2025) studied this question.

synapsesocial.com/papers/68d434ef713b0b5dfea74ad9https://doi.org/10.1101/2025.09.11.675705
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Robust CRISPR Screens Identify TPL1 as a Novel Long Noncoding RNA Driving Triple-Negative Breast Cancer Hallmarks2025
  2. 2Targeting mitochondrial proteases CLPP and LONP1 via disruption of mitochondrial redox homeostasis induces proteotoxic stress and suppresses tumor progression2025
  3. 3SMALL MOLECULE CLPP ACTIVATORS IMPAIR MITOCHONDRIAL FUNCTIONS AND INDUCE SENESCENCE IN TRIPLE-NEGATIVE BREAST CANCER2026
  4. 4TRP channels and cancer modulation: a voyage beyond metabolic reprogramming, oxidative stress and the advent of nanotechnologies in targeted therapy2025
  5. 5Integrative proteogenomics and forward genetics reveals a novel mitotic vulnerability in triple-negative breast cancer.2025