Evidence for intrathecal sodium butyrate as a novel option for leptomeningeal metastasis

Nakagawa, Hidemitsu; Yui, Yoshihiro; Sasagawa, Satoru; Itoh, Kazuyuki

doi:10.1007/s11060-018-2852-2

Cited by 3 publications

(3 citation statements)

References 37 publications

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“…7 Many studies show that NaB acts as a negative regulator in various types of cancer. [8][9][10] NaB has been found to inhibit cell proliferation and migration of colorectal cancer, promote CRC cell apoptosis and induce autophagy and cell death. [10][11][12][13][14] The previously reported the correlation between NaB and Oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

<p>Sodium Butyrate Selectively Kills Cancer Cells and Inhibits Migration in Colorectal Cancer by Targeting Thioredoxin-1</p>

Wang¹,

Fang²,

Zhang³

et al. 2020

OTT

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Background: Sodium butyrate (NaB) is a short-chain fatty acid which is produced by bacterial fermentation of nondigestible dietary fiber and has been reported to exert anti-tumor effects in many tumors including colorectal cancer (CRC). However, the role of thioredoxin-1 (Trx-1) in NaB-induced anti-tumor effect has not been completely clarified. Materials and Methods: Effects of NaB on the growth of CRC cell lines HT29 and SW480 were detected by the Cell Counting Kit-8 (CCK-8) and colony formation assays. The apoptotic cells were determined by flow cytometry, and cell migration was assessed by a Transwell assay. Western blot analysis was used to test the Trx-1 and epithelial-to-mesenchymal transition (EMT)-related proteins level. Reactive oxygen species (ROS) level was determined and N-acetylcysteine (NAC) recovery experiment was performed in CRC cells. In addition, mice xenograft model was established to test the effect of NaB on CRC growth in vivo. Further, the effects of NaB on CRC cells with overexpression or knockdown were tested by the CCK-8 and Transwell assays. Results: NaB treatment significantly inhibited cell growth and decreased Trx-1 protein expression in CRC cells but not in normal colon epithelial cells. NaB also induced apoptosis, inhibited colony formation, migration and EMT in CRC cells. Besides, NaB increased ROS level in CRC cells and NAC reversed NaB-induced inhibition of cell proliferation. Moreover, downregulation of Trx-1 significantly enhanced NaB-induced inhibitory effects on cell growth and migration, whereas overexpression of Trx-1 attenuated NaB-induced inhibitory effects on growth and migration in CRC cells. Conclusion: These findings indicate that the NaB-mediated anti-tumor effects on CRC cells are related to downregulation of Trx-1.

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Section: Introductionmentioning

confidence: 99%

<p>Sodium Butyrate Selectively Kills Cancer Cells and Inhibits Migration in Colorectal Cancer by Targeting Thioredoxin-1</p>

Wang¹,

Fang²,

Zhang³

et al. 2020

OTT

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“…Though it is generally well tolerated, it can cause an acute cerebritis leading to clinical symptoms including headache as well as potentially an encephalitis. 41 However, to date, IT approaches have proven to be of limited therapeutic efficacy due to bulky deposits of tumor which drugs in the CSF cannot penetrate. 1 Two other constraints are that clinical trial data are limited for IT therapy 4 and we lack a basic understanding of the pathophysiology of LMD.…”

Section: Current Limitationsmentioning

confidence: 99%

“…4 Several agents have been used as IT treatment for LMD. Commonly used agents include methotrexate, thiotepa (an alkylating agent) and cytarabine (a pyrimidine analog), 4 25 27 37 41 trastuzumab (an anti-HER2 therapy), and topotecan (a topoisomerase I inhibitor). 37 42 There is also an ongoing trial examining the use of a novel IT iron-chelation treatment for patients with LMD (NCT05184816).…”

Section: Treatment Strategiesmentioning

confidence: 99%

Leptomeningeal Carcinomatosis from Solid Tumor Malignancies: Treatment Strategies and Biomarkers

Malani,

Bhatia,

Warner

et al. 2023

Semin Neurol

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Leptomeningeal metastases/diseases (LMDs) are a late-stage complication of solid tumor or hematologic malignancies. LMD is spread of cancer cells to the layers of the leptomeninges (pia and arachnoid maters) and subarachnoid space seen in 3 to 5% of cancer patients. It is a disseminated disease which carries with it significant neurologic morbidity and mortality. Our understanding of disease pathophysiology is currently lacking; however, advances are being made. As our knowledge of disease pathogenesis has improved, treatment strategies have evolved. Mainstays of treatment such as radiotherapy have changed from involved-field radiotherapy strategies to proton craniospinal irradiation which has demonstrated promising results in recent clinical trials. Systemic treatment strategies have also improved from more traditional chemotherapeutics with limited central nervous system (CNS) penetration to more targeted therapies with better CNS tumor response. Many challenges remain from earlier clinical detection of disease through improvement of active treatment options, but we are getting closer to meaningful treatment.

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Management of leptomeningeal carcinomatosis and challenges of trial design

Gill

Brastianos

2019

Current Opinion in Oncology

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Purpose of review Highlight recent data in lung and breast cancer leptomeningeal disease and address clinical trials that are open for patients. Recent findings Patients with lung and breast cancer leptomeningeal disease have survival outcomes of less than 1 year, despite advances in treatment strategy. Efforts to develop liquid biopsy biomarkers of disease progression from cerebrospinal fluid and plasma are underway. There are over 10 clinical trials open for patients with leptomeningeal disease, half of which use immunotherapy. Summary Consortium-based, multicenter clinical trials for patients with leptomeningeal disease are urgently needed to expand the treatment armamentarium.

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Evidence for intrathecal sodium butyrate as a novel option for leptomeningeal metastasis

Abstract: Continuous intrathecal SB administration significantly improved prognoses in a rat LM model, which suggests that SB is a promising therapy for LM.

Cited by 3 publications

References 37 publications

<p>Sodium Butyrate Selectively Kills Cancer Cells and Inhibits Migration in Colorectal Cancer by Targeting Thioredoxin-1</p>

<p>Sodium Butyrate Selectively Kills Cancer Cells and Inhibits Migration in Colorectal Cancer by Targeting Thioredoxin-1</p>

Leptomeningeal Carcinomatosis from Solid Tumor Malignancies: Treatment Strategies and Biomarkers

Management of leptomeningeal carcinomatosis and challenges of trial design

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