Boric acid suppresses cell proliferation by TNF signaling pathway mediated apoptosis in SW-480 human colon cancer line

Sevimli, Murat; Bayram, Dilek; Özgöçmen, Meltem; Armağan, İlkay; Sevimli, Tuğba Semerci

doi:10.1016/j.jtemb.2022.126958

Cited by 22 publications

(14 citation statements)

References 33 publications

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“…The TNF signaling pathway mediates apoptosis in SW480 cells. It has been reported that boric acid treatment activates the TNF signaling pathway, which, in turn, induces apoptosis in SW480 cells, and the qRT-PCR results showed that the expression levels of TNF and TNFSF8 genes in the treatment group were significantly upregulated ( Sevimli et al, 2022 ). However, the expression levels of these two genes were not significantly altered in our transcriptomic analysis.…”

Section: Discussionmentioning

confidence: 99%

Plantaricin BM-1 decreases viability of SW480 human colorectal cancer cells by inducing caspase-dependent apoptosis

et al. 2023

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Plantaricin BM-1 is a class IIa bacteriocin produced by Lactobacillus plantarum BM-1 that has significant antimicrobial activity against food-borne bacteria. In this study, a cell proliferation assay and scanning electron microscopy were used to detect changes in the viability of SW480, Caco-2, and HCT-116 colorectal cancer cells treated with plantaricin BM-1. We found that plantaricin BM-1 significantly reduced the viability of all colorectal cancer cell lines tested, especially that of the SW480 cells. Scanning electron microscopy showed that plantaricin BM-1 treatment reduced the number of microvilli and slightly collapsed the morphology of SW480 cells. Fluorescence microscopy and flow cytometry demonstrated that plantaricin BM-1 induced apoptosis of SW480 cells in a concentration-dependent manner. Western blotting further showed that plantaricin BM-1-induced apoptosis of SW480 cells was mediated by the caspase pathway. Finally, transcriptomic analysis showed that 69 genes were differentially expressed after plantaricin BM-1 treatment (p < 0.05), of which 65 were downregulated and four were upregulated. The Kyoto Encyclopedia of Genes and Genomes enrichment analysis showed that expression levels of genes involved in the TNF, NF-κB, and MAPK signaling pathways, as well as functional categories such as microRNAs in cancer and transcriptional misregulation in cancer, were affected in SW480 cells following the treatment with plantaricin BM-1. In conclusion, plantaricin BM-1 induced death in SW480 cells via the caspase-dependent apoptosis pathway. Our study provides important information for further development of plantaricin BM-1 for potential applications in anti-colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Plantaricin BM-1 decreases viability of SW480 human colorectal cancer cells by inducing caspase-dependent apoptosis

et al. 2023

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“…Ek olarak, fenilboronik asit, guanidin biborik asit, dihidroksi bor hidroklorür monohidrat, borik asit ve sodyum tetraborat gibi bor türevi bileşiklerin B16F10 murin melanomu, HL-60 ve U-937 insan lösemi hücreleri üzerinde sitotoksik etkileri olduğu belgelenmiştir (22,23). Bir başka çalışmada, borik asidin insan prostat kanseri ve insan kolon adenokarsinom hücreleri proliferasyonu üzerindeki inhibisyonunu araştırmak için borik asit içeren besiyeri eklenmiş ve daha sonra hücrelerde proliferasyon, apoptoz, hücre döngüsü ve mitokondriyal aktivasyon açısından DU145, LNCaP, PC3 ve SW-480 kanser hücre hatlarında doza bağlı olarak hücre proliferasyonunu açıkça azalttığı tespit edilmiştir (24,25). Benzer şekilde, daha önce bir çalışmamızda borik asidin DU-145 kanser hücrelerinde konsantrasyona bağlı olarak proliferasyonu engellemiş ve morfolojik deformitelere ve oksidan stresi arttırarak da apoptoza neden olduğunu bulduk (26).…”

Section: Hücre Canlılığı Analiziunclassified

Cytotoxic Effects of Borax via GPx4/ACSL4 Signaling Pathway in Colorectal Cancer Cells

Hacıoğlu

Davran

2023

Sağlık Bilimlerinde Değer

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Amaç: Kolorektal kanser (CRC), kansere bağlı ölümlerin yaklaşık %10'unu oluşturmasıyla, malignite yönünden üçüncü ve kansere bağlı ölümlerde ikinci sırada yer almaktadır. Ferroptoz, CRC dahil çok sayıda kanserin tedavisinde ilaç direncini önlemede terapötiklerin anti-kanser etkinliğini arttırabilecek potansiyel demire bağlı hücre ölüm yolağıdır. Bu çalışmada CRC hücrelerinde ferroptozu sinyal yolağı üzerinden boraksın anti-proliferatif etkilerini araştırmak amaçlandı. Gereç ve Yöntemler: Öncelikle, boraksın sitotoksik konsantrasyonları (0-64 mM aralığında) 3-(4,5-dimetiltiazol-2-il)-2,5-difenil tetrazolyum bromür (MTT) testi ile belirlendi. Daha sonra sitotoksik boraks konsantrasyonları ile 24 saat inkübe edilen HCT-116 hücrelerinde glutatyon peroksidaz 4 (GPx4), açil-KoA sentetaz uzun zincirli aile üyesi 4 (ACSL4), malondialdehit (MDA) ve 8-hidroksideoksiguanozin (8-OHdG) seviyeleri belirlendi. Bulgular: 1 ve 4 mM boraks konsantrasyonları hücre canlılığını etkilemezken, 8 mM ve üzerindeki boraks konsantrasyonları HTC-116 hücrelerinde canlılığı anlamlı şekilde düşürmüştür (p

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“…Previous in vivo and in vitro studies have demonstrated the anti-cancer effects of boron. These effects are also observed in prostate cancer, [29] colon cancer, [28] lung cancer, [30] breast cancer, [31] and malignant melanoma. [32][33][34] Chemotherapeutic agents, while effective against cancer cells, can also induce toxic effects on healthy cells.…”

Section: Introductionmentioning

confidence: 95%

“…Research has shown that boric acid induces effects such as oxidative stress, apoptosis, and inhibition of cell growth in cancer cell lines. [25][26][27][28] Boron, in various forms, has demonstrated distinctive anticancer properties that encompass multiple mechanisms. BA, a form of boron, has been shown to induce apoptosis, which is the programmed cell death of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Designing of Polymeric Nanoparticles for Enhanced Breast Cancer Therapy: Combining Paclitaxel, Boric Acid and Tannic Acid for Controlled Drug Delivery

Kaya,

Solak,

Doğan

et al. 2024

ChemistrySelect

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This study introduces an innovative approach to enhance breast cancer treatment by combining Boric Acid (BA) and Tannic Acid (TA) with Paclitaxel (PTX) within gelatin/sodium alginate (Gel/NaAlg) nanoparticles, resulting in a synergistic combination therapy. The methodology involved integrating PTX, TA, and BA into the polymeric framework using an emulsion cross‐linking method. The resulting nanoparticles underwent rigorous characterization, confirming their suitability as a controlled release platform. Techniques such as Scanning Electron Microscope (SEM), Differential Scanning Calorimetry (DSC), X‐ray Diffractometry (XRD), and Fourier Transform Infrared Spectroscopy (FTIR) were employed for thorough analysis. The synthesized nanoparticles demonstrated a size below 204 nm, and extensive analyses confirmed their structural integrity and composition. Notably, Gel/NaAlg/PTX/BA/TA nanoparticles exhibited superior drug release kinetics compared to other formulations, offering a promising strategy for controlled release of hydrophobic drugs like PTX. Entrapment efficiency ranged from 49.84 % to 63.38 %, and drug loading capacities spanned from 49.81 to 61.42 μg/mg. This study pioneers a novel approach in breast cancer therapy by incorporating BA and TA into PTX‐loaded Gel/NaAlg nanoparticlesThese findings emphasize the importance of continued exploration in innovative drug delivery systems for more effective cancer interventions.

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Boric acid suppresses cell proliferation by TNF signaling pathway mediated apoptosis in SW-480 human colon cancer line

Cited by 22 publications

References 33 publications

Plantaricin BM-1 decreases viability of SW480 human colorectal cancer cells by inducing caspase-dependent apoptosis

Plantaricin BM-1 decreases viability of SW480 human colorectal cancer cells by inducing caspase-dependent apoptosis

Cytotoxic Effects of Borax via GPx4/ACSL4 Signaling Pathway in Colorectal Cancer Cells

Designing of Polymeric Nanoparticles for Enhanced Breast Cancer Therapy: Combining Paclitaxel, Boric Acid and Tannic Acid for Controlled Drug Delivery

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