Lithium in Cancer Therapy: Friend or Foe?

Yang, Chunhao; Zhu, Bo; Zhan, Mingjie; Hua, Zichun

doi:10.3390/cancers15041095

Cited by 13 publications

(5 citation statements)

References 154 publications

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“…In addition to the current use of lithium in the therapy of bipolar disorders, lithium is also being investigated as a drug for experimental cancer therapy. It was found that lithium has the various antitumor effects in cancer models in vitro and in vivo (Villegas‐Vázquez et al, 2023; Yang et al, 2023); however, the data regarding lithium accumulation in tumors are limited. Previously, we have revealed that lithium carbonate accumulates in the tumor at a concentration higher than 20 μg/g in B16 mouse melanoma model in vivo (Taskaeva et al, 2023); nevertheless, it is not clear whether accumulation is the same for different melanoma cell lines or other cell lines.…”

Section: Discussionmentioning

confidence: 99%

Lithium salts cytotoxicity and accumulation in melanoma cells in vitro

Taskaeva,

Kasatova,

Razumov

et al. 2023

J of Applied Toxicology

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Boron neutron capture therapy is a perspective selective technology for the destruction of cancer cells, while the use of lithium instead of boron may represent a new and promising vector for the development of neutron capture therapy (NCT). The aim of the study was a comparative assessment of the cytotoxicity of various lithium salts, as well as an analysis of the accumulation of lithium in tumor cells in vitro to determine the possibility of using lithium in NCT. The cytotoxicity of lithium salts was determined using MTT‐test and colony forming assay on human fibroblasts BJ‐5ta, human skin melanoma SK‐Mel‐28, and mouse skin melanoma B16 cell lines. An assessment of lithium concentration in cells was performed using inductively coupled plasma atomic emission spectrometry. Our results showed that three different lithium salts at a concentration of 40 μg/ml are not toxic for both tumor and normal cells. The highest uptake values were obtained on murine melanoma B16 cells when exposed to lithium carbonate (0.8 μg/106 cells); however, human melanoma SK‐Mel‐28 cells effectively accumulated both lithium carbonate and lithium citrate (about 0.46 μg/106 cells for two salts). Thus, our results demonstrate a range of non‐toxic doses of lithium salts and a high uptake of lithium by tumor cells, which indicates the possibility to use the lithium in NCT.

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Section: Discussionmentioning

confidence: 99%

Lithium salts cytotoxicity and accumulation in melanoma cells in vitro

Taskaeva,

Kasatova,

Razumov

et al. 2023

J of Applied Toxicology

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“…Similarly, ginsenoside Rb1 promotes autophagy in colon cancer cells through the generation of reactive oxygen species and activation of the JNK signaling pathway (Kim 2013 ). Lithium induces autophagy along with autophagosomes and autophagic lysosomes in several cancers, including melanoma, hepatocellular carcinoma, cervical carcinoma, and renal carcinoma (Yang et al 2023 ). Lithium agents such as lithium acetoacetate (LiAcAc), lithium chloride (LiCl), lithium citrate (Li 3 C 6 H 5 O 7 ) and lithium carbonate (Li 2 CO 3 ) can be used to induce autophagy and thus inhibit tumor growth (Villegas-Vázquez et al 2023 ).…”

Section: Application Of Autophagy Inducersmentioning

confidence: 99%

The multiple roles of autophagy in uveal melanoma and the microenvironment

Liu,

Yao,

Shang

et al. 2024

J Cancer Res Clin Oncol

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Purpose Uveal melanoma (UM) is the most common primary malignant intraocular tumor in adults, and effective clinical treatment strategies are still lacking. Autophagy is a lysosome-dependent degradation system that can encapsulate abnormal proteins, damaged organelles. However, dysfunctional autophagy has multiple types and plays a complex role in tumorigenicity depending on many factors, such as tumor stage, microenvironment, signaling pathway activation, and application of autophagic drugs. Methods A systematic review of the literature was conducted to analyze the role of autophagy in UM, as well as describing the development of autophagic drugs and the link between autophagy and the tumor microenvironment. Results In this review, we summarize current research advances regarding the types of autophagy, the mechanisms of autophagy, the application of autophagy inhibitors or agonists, autophagy and the tumor microenvironment. Finally, we also discuss the relationship between autophagy and UM. Conclusion Understanding the molecular mechanisms of how autophagy differentially affects tumor progression may help to design better therapeutic regimens to prevent and treat UM.

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“…Lithium inhibits IMPase to induce mTOR-independent autophagy. Simultaneously, it inhibits GSK-3β, which, in turn, reduces autophagy by activating mTOR 33 , 34 . The differential effects of lithium on autophagy may be attributed to varying therapeutic concentrations 35 .…”

Section: Molecular Mechanismmentioning

confidence: 99%

Exploring the Neuroprotective Effects of Lithium in Ischemic Stroke: A literature review

Wang,

Lu,

Shi

et al. 2024

Int. J. Med. Sci.

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Ischemic stroke ranks among the foremost clinical causes of mortality and disability, instigating neuronal degeneration, fatalities, and various sequelae. While standard treatments, such as intravenous thrombolysis and endovascular thrombectomy, prove effective, they come with limitations. Hence, there is a compelling need to develop neuroprotective agents capable of improving the functional outcomes of the nervous system. Numerous preclinical studies have demonstrated that lithium can act in multiple molecular pathways, including glycogen synthase kinase 3(GSK-3), the Wnt signaling pathway, the mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) signaling pathway, brain-derived neurotrophic factor (BDNF), mammalian target of rapamycin (mTOR), and glutamate receptors. Through these pathways, lithium has been shown to affect inflammation, autophagy, apoptosis, ferroptosis, excitotoxicity, and other pathological processes, thereby improving central nervous system (CNS) damage caused by ischemic stroke. Despite these promising preclinical findings, the number of clinical trials exploring lithium's efficacy remains limited. Additional trials are imperative to thoroughly ascertain the effectiveness and safety of lithium in clinical settings. This review delineates the mechanisms underpinning lithium's neuroprotective capabilities in the context of ischemic stroke. It elucidates the intricate interplay between these mechanisms and sheds light on the involvement of mitochondrial dysfunction and inflammatory markers in the pathophysiology of ischemic stroke. Furthermore, the review offers directions for future research, thereby advancing the understanding of the potential therapeutic utility of lithium and establishing a theoretical foundation for its clinical application.

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Lithium in Cancer Therapy: Friend or Foe?

Cited by 13 publications

References 154 publications

Lithium salts cytotoxicity and accumulation in melanoma cells in vitro

Lithium salts cytotoxicity and accumulation in melanoma cells in vitro

The multiple roles of autophagy in uveal melanoma and the microenvironment

Exploring the Neuroprotective Effects of Lithium in Ischemic Stroke: A literature review

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