Corrigendum: Dihydroartemisinin Induces Growth Arrest and Overcomes Dexamethasone Resistance in Multiple Myeloma

Chen, Ying; Li, Rui; Zhu, Yuqi; Zhong, Sixia; Qian, Jinjun; Yang, Dongqing; Jurczyszyn, Artur; Beksaç, Meral; Gu, Chunyan; Yang, Ye

doi:10.3389/fonc.2021.736373

Cited by 2 publications

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“…DHA was previously shown to prevent laryngeal cancer metastases through signal transducer and activator of transcription 3 (STAT3) inactivation (Wang, Sun, et al., 2020), with activated STAT3 shown to interact with the MCU N‐terminal domain in cardiomyocytes following ischaemia/reperfusion injury to alleviate mitochondrial Ca 2+ overload (Wu, Tan, et al., 2019). Given that DHA has not been identified as a direct inhibitor of mtCU, it may function by decreasing the ΔΨ m and reducing mtCU component expression as a result of altering various transcriptional, translational and/or degradative pathways (Chen et al., 2021; Zheng et al., 2022; Zhu et al., 2018). DHA induced a dose‐dependent decrease in ΔΨ m after 48 h in JF‐305 pancreatic cancer cells, positively correlated with increased intracellular ROS generation (Zhu et al., 2018).…”

Section: Introductionmentioning

confidence: 99%

The mitochondrial calcium uniporter: Balancing tumourigenic and anti‐tumourigenic responses

Colussi,

Stathopulos

2024

The Journal of Physiology

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Increased malignancy and poor treatability associated with solid tumour cancers have commonly been attributed to mitochondrial calcium (Ca2+) dysregulation. The mitochondrial Ca2+ uniporter complex (mtCU) is the predominant mode of Ca2+ uptake into the mitochondrial matrix. The main components of mtCU are the pore‐forming mitochondrial Ca2+ uniporter (MCU) subunit, MCU dominant‐negative beta (MCUb) subunit, essential MCU regulator (EMRE) and the gatekeeping mitochondrial Ca2+ uptake 1 and 2 (MICU1 and MICU2) proteins. In this review, we describe mtCU‐mediated mitochondrial Ca2+ dysregulation in solid tumour cancer types, finding enhanced mtCU activity observed in colorectal cancer, breast cancer, oral squamous cell carcinoma, pancreatic cancer, hepatocellular carcinoma and embryonal rhabdomyosarcoma. By contrast, decreased mtCU activity is associated with melanoma, whereas the nature of mtCU dysregulation remains unclear in glioblastoma. Furthermore, we show that numerous polymorphisms associated with cancer may alter phosphorylation sites on the pore forming MCU and MCUb subunits, which cluster at interfaces with EMRE. We highlight downstream/upstream biomolecular modulators of MCU and MCUb that alter mtCU‐mediated mitochondrial Ca2+ uptake and may be used as biomarkers or to aid in the development of novel cancer therapeutics. Additionally, we provide an overview of the current small molecule inhibitors of mtCU that interact with the Asp residue of the critical Asp‐Ile‐Met‐Glu motif or through other allosteric regulatory mechanisms to block Ca2+ permeation. Finally, we describe the relationship between MCU‐ and MCUb‐mediating microRNAs and mitochondrial Ca2+ uptake that should be considered in the discovery of new treatment approaches for cancer. image

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Section: Introductionmentioning

confidence: 99%

The mitochondrial calcium uniporter: Balancing tumourigenic and anti‐tumourigenic responses

Colussi,

Stathopulos

2024

The Journal of Physiology

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“…The latest clinical MM therapy is a new immunomodulatory therapy using chimeric antigen receptor T cells, bispecific T cell conjugates, and immune checkpoint inhibitors (6). Although the therapeutic armamentarium for MM has continued to evolve (7)(8)(9)(10)(11)(12)(13)(14), MM still possesses the characteristics of high relapse and incurability. It is necessary to explore more effective therapies to improve MM prognosis significantly.…”

Section: Introductionmentioning

confidence: 99%

Acupuncture Synergized With Bortezomib Improves Survival of Multiple Myeloma Mice via Decreasing Metabolic Ornithine

Qian

Feng

et al. 2021

Front. Oncol.

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Multiple myeloma (MM) is a hematological malignancy worldwide in urgent need for novel therapeutic strategies. Since Velcade (bortezomib) was approved for the treatment of relapsed/refractory MM in 2003, we have seen considerable improvement in extending MM patient survival. However, most patients are fraught with high recurrence rate and incurability. Acupuncture is known for alleviating patient symptoms and improving the quality of life, but it is not well investigated in MM, especially in combination with bortezomib. In this study, we employed LC-MS and UHPLC-MS together with bioinformatics methods to test serum samples from 5TMM3VT MM murine model mice with four different treatments [control (C) group, bortezomib (V) treatment group, acupuncture (A) group, and combined (VA) group]. MM mice in group VA had longer survival time than mice in group A or group V. Joint pathway analysis indicated the underlying arginine and proline metabolism pathway among the 32 significantly decreased metabolites in group VA. CCK-8 assay and in vivo experiments validated that ornithine, the metabolite of arginine, promoted MM cell proliferation. In addition, gene expression omnibus (GEO) database analysis suggested that MM patients with higher ornithine decarboxylase 1 (ODC1) expression were evidently associated with poor overall survival. In summary, this study demonstrates the synergistic effects of acupuncture and bortezomib on extending the survival of MM model mice and provides potential therapeutic targets in the treatment of MM.

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Corrigendum: Dihydroartemisinin Induces Growth Arrest and Overcomes Dexamethasone Resistance in Multiple Myeloma

Cited by 2 publications

References 0 publications

The mitochondrial calcium uniporter: Balancing tumourigenic and anti‐tumourigenic responses

The mitochondrial calcium uniporter: Balancing tumourigenic and anti‐tumourigenic responses

Acupuncture Synergized With Bortezomib Improves Survival of Multiple Myeloma Mice via Decreasing Metabolic Ornithine

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