We are analyzing https://link.springer.com/article/10.1007/s11010-024-05054-5.

Title:
Lysosomal cation channel TRPML1 suppression sensitizes acute myeloid leukemia cells to chemotherapeutics by inhibiting autophagy | Molecular and Cellular Biochemistry
Description:
Despite the implementation of novel therapeutic regimens and extensive research efforts, chemoresistance remains a formidable challenge in the treatment of acute myeloid leukemia (AML). Notably, the involvement of lysosomes in chemoresistance has sparked interest in developing lysosome-targeted therapies to sensitize tumor cells to currently approved chemotherapy or as innovative pharmacological approaches. Moreover, as ion channels on the lysosomal membrane are critical regulators of lysosomal function, they present potential as novel targets for enhancing chemosensitivity. Here, we discovered that the expression of a lysosomal cation channel, namely transient receptor potential mucolipin 1 (TRPML1), was elevated in AML cells. Inhibiting TRPML1 individually does not impact the proliferation and apoptosis of AML cells. Importantly, inhibition of TRPML1 demonstrated the potential to modulate the sensitivity of AML cells to chemotherapeutic agents. Exploration of the underlying mechanisms revealed that suppression of TRPML1 impaired autophagy while concurrently increasing the production of reactive oxygen species (ROS) and ROS-mediated lipid peroxidation (Lipid-ROS) in AML cells. Finally, the knockdown of TRPML1 significantly reduced OCI-AML3 tumor growth following chemotherapy in a mouse model of human leukemia. In summary, targeting TRPML1 represents a promising approach for combination therapy aimed at enhancing chemosensitivity in treating AML.
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Keywords {🔍}

pubmed, google, scholar, cas, central, cell, leukemia, autophagy, acute, myeloid, lysosomal, trpml, cells, article, channel, china, wang, science, research, aml, cang, biol, medicine, hefei, data, cancer, chunlei, access, nature, function, manuscript, lysosomes, potential, ros, author, blood, national, university, technology, anhui, privacy, cookies, content, dai, lin, xingbing, chemoresistance, treatment, ion, channels,

Topics {✒️}

leukemia cooperative group lysosomal cation channel cellular biochemistry aims month download article/chapter acute myeloid leukemia developing lysosome-targeted therapies xingbing wang designed cryo-electron microscopy structure pi3k/akt/pten pathway acute myleogenous leukemia xingbing wang overcomes stroma-mediated chemoresistance chunlei cang aml promotes proliferation targeting trpml1 represents trpml1 impaired autophagy lysosomal ca2+ release sensitize tumor cells ros-mediated lipid peroxidation hefei national laboratory author information authors mammalian tpc1 channel common transcriptional programs characterize ion channels lysosome-mediated chemoresistance inhibiting trpml1 individually privacy choices/manage cookies lili qu participated lysosomal drug sequestration mcoln1 promotes proliferation full article pdf induction-consolidation chemotherapy enhancing chemosensitivity negatively regulating mapk front-line chemotherapeutics wenping zeng contributed miaomiao wu participated ion channel type iv mucolipidosis pore na+ channels mucolipidosis type iv intracellular sequestration site chronic disease check access instant access herzik ma jr nox proteinin diseases holds exclusive rights extensive research efforts innovative pharmacological approaches

Questions {❓}

Kallunki T, Olsen OD, Jaattela M (2013) Cancer-associated lysosomal changes: friends or foes?

Schema {🗺️}

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         description:Despite the implementation of novel therapeutic regimens and extensive research efforts, chemoresistance remains a formidable challenge in the treatment of acute myeloid leukemia (AML). Notably, the involvement of lysosomes in chemoresistance has sparked interest in developing lysosome-targeted therapies to sensitize tumor cells to currently approved chemotherapy or as innovative pharmacological approaches. Moreover, as ion channels on the lysosomal membrane are critical regulators of lysosomal function, they present potential as novel targets for enhancing chemosensitivity. Here, we discovered that the expression of a lysosomal cation channel, namely transient receptor potential mucolipin 1 (TRPML1), was elevated in AML cells. Inhibiting TRPML1 individually does not impact the proliferation and apoptosis of AML cells. Importantly, inhibition of TRPML1 demonstrated the potential to modulate the sensitivity of AML cells to chemotherapeutic agents. Exploration of the underlying mechanisms revealed that suppression of TRPML1 impaired autophagy while concurrently increasing the production of reactive oxygen species (ROS) and ROS-mediated lipid peroxidation (Lipid-ROS) in AML cells. Finally, the knockdown of TRPML1 significantly reduced OCI-AML3 tumor growth following chemotherapy in a mouse model of human leukemia. In summary, targeting TRPML1 represents a promising approach for combination therapy aimed at enhancing chemosensitivity in treating AML.
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      description:Despite the implementation of novel therapeutic regimens and extensive research efforts, chemoresistance remains a formidable challenge in the treatment of acute myeloid leukemia (AML). Notably, the involvement of lysosomes in chemoresistance has sparked interest in developing lysosome-targeted therapies to sensitize tumor cells to currently approved chemotherapy or as innovative pharmacological approaches. Moreover, as ion channels on the lysosomal membrane are critical regulators of lysosomal function, they present potential as novel targets for enhancing chemosensitivity. Here, we discovered that the expression of a lysosomal cation channel, namely transient receptor potential mucolipin 1 (TRPML1), was elevated in AML cells. Inhibiting TRPML1 individually does not impact the proliferation and apoptosis of AML cells. Importantly, inhibition of TRPML1 demonstrated the potential to modulate the sensitivity of AML cells to chemotherapeutic agents. Exploration of the underlying mechanisms revealed that suppression of TRPML1 impaired autophagy while concurrently increasing the production of reactive oxygen species (ROS) and ROS-mediated lipid peroxidation (Lipid-ROS) in AML cells. Finally, the knockdown of TRPML1 significantly reduced OCI-AML3 tumor growth following chemotherapy in a mouse model of human leukemia. In summary, targeting TRPML1 represents a promising approach for combination therapy aimed at enhancing chemosensitivity in treating AML.
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      name:Department of Hematology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China
      name:CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:Department of Hematology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:Department of Hematology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China
      name:Division of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Technology of China, Hefei, China
      name:CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Basic Medical Sciences, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
      name:Department of Rheumatology and Immunology, The First Affiliated Hospital of USTC, University of Science and Technology of China, Hefei, China
      name:Institute of Health and Medicine, Hefei Comprehensive National Science Center, Hefei, China
      name:Department of Hematology, Centre for Leading Medicine and Advanced Technologies of IHM, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China
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