Ciprofloxacin mediates cancer stem cell phenotypes in lung cancer cells through caveolin-1-dependent mechanism

Phiboonchaiyanan, Preeyaporn Plaimee; Kiratipaiboon, Chayanin; Chanvorachote, Pithi

doi:10.1016/j.cbi.2016.03.005

Cited by 25 publications

(26 citation statements)

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“…Spheroids Formation Assay. Spheroids were grown using the adjusted method from Chanvorachote and Luanpitpong (2016), Phiboonchaiyanan et al (2016), and Powan et al (2017). Human NSCLC-derived cells (H460 and A549) and primary DP1 cells were pretreated with Ti 0.8 O 2 nanosheets at nontoxic concentrations (0-1 mg/ml) for 48 hours at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…For CSC-rich population formation, the method was slightly modified from a previously described method (Chanvorachote and Luanpitpong, 2016;Phiboonchaiyanan et al, 2016;Powan et al, 2017). Cells were seeded onto a 24-well ultralow-attachment plate, with approximately 2.5 Â 10 3 cells/well in 0.8% methylcellulose-based serum-free medium supplemented with 20 ng/ml epidermal growth factor, basic fibroblast growth factor, and 4 mg/ml insulin.…”

Section: Methodsmentioning

confidence: 99%

“…Just as in normal tissue stem cells, several cell-signaling pathways have been implicated in mechanisms underlying stemness in CSCs. Protein kinase B (Akt), b-catenin, and Notch signals have been shown to be key regulatory mechanisms underlying stemness in both normal and cancerous stem cells (Hadjimichael et al, 2015;Mohammed et al, 2016;Phiboonchaiyanan et al, 2016;Koury et al, 2017). To clarify the possible effects of nanosheets on such stem cell pathways, we determined the levels of related proteins in nanosheettreated cells.…”

Section: Characterizationmentioning

confidence: 99%

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Ti_0.8O₂Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

et al. 2019

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Recent research into the cancer stem cell (CSC) concept has driven progress in the understanding of cancer biology and has revealed promising CSC-specific targets for drug discovery efforts. As malignancies of lung cancer have been shown to be strongly associated with activities of CSCs, we examined the effects of Ti 0.8 O 2 nanosheets on these cells. Here we show that the nanosheets target lung CSCs but not normal primary dermal papilla (DP) stem cells. Whereas Ti 0.8 O 2 caused a dramatic apoptosis along with a decrease in CSC phenotypes, in primary human DP cells such effects of nanosheets have been minimal. Nanosheets reduced the ability of lung cancer cells to generate three-dimensional tumor spheroids, lung CSC markers (CD133 and ALDH1A1), and CSC transcription factors (Nanog and Oct-4). Ti 0.8 O 2 nanosheets reduced CSC signaling through mechanisms involving suppression of protein kinase B (AKT) and Notch-1 pathways. In addition, the nanosheets inhibited the migration and invasive activities of lung cancer cells and reduced epithelial-to-mesenchymal transition (EMT) markers as N-cadherin, vimentin, and Slug, as well as metastasis-related integrins (integrin-av and integrin-b1). Importantly, we found that the selectivity of the Ti 0.8 O 2 nanosheets in targeting cancer cells was mediated by induction of cellular superoxide anion in cancerous but not normal cells. Inhibition of nanosheet-induced superoxide anion restored the suppression of CSC and EMT in cancer cells. These findings demonstrate a promising distinctive effect of Ti 0.8 O 2 nanosheets on lung CSC that may lead to opportunities to use such a nanomaterial in cancer therapy.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Characterizationmentioning

confidence: 99%

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Ti_0.8O₂Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

et al. 2019

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“…For CSC-rich population establishment, the spheroid culture assay used in this study was slightly modified from a previously described method (Cao et al, 2011;Bao et al, 2013;Thakur et al, 2015;Weiswald et al, 2015;Yongsanguanchai et al, 2015;Phiboonchaiyanan et al, 2016;Shaheen et al, 2016). Cells were seeded onto a 24-well ultralow attachment plate, with approximately 2.5 Â 10 3 cells/well in 0.8% methylcellulose-based serum-free medium supplemented with 20 ng/ml epidermal growth factor, basic fibroblast growth factor, and 4 mg/ml insulin.…”

Section: Methodsmentioning

confidence: 99%

Cancer Stem Cell–Suppressing Activity of Chrysotoxine, a Bibenzyl fromDendrobium pulchellum

Bhummaphan

Pongrakhananon

Sritularak

et al. 2017

J Pharmacol Exp Ther

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Cancer stem cells (CSCs) have been recognized as rare populations driving cancer progression, metastasis, and drug resistance in leading cancers. Attempts have been made toward identifying compounds that specifically target these CSCs. Therefore, investigations of novel therapeutic strategies for CSC targeting are required. The cytotoxic effects of chrysotoxine on human non-small cell lung cancer-derived H460 and H23 cells were evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The effects of chrysotoxine suppression of CSC-like phenotypes were determined in CSC-rich populations and primary CSCs in three-dimensional (3D) culture and in an extreme limiting dilution assay. Expression of CSC markers and associated proteins was determined by Western blot analyse and flow cytometry. We have reported herein the CSC-suppressing activity of chrysotoxine, a bibenzyl compound isolated from We have shown, to our knowledge for the first time, that chrysotoxine dramatically suppresses CSC-like phenotypes of H460 and H23 cells. Treatment with chrysotoxine significantly reduced the viability of 3D CSC-rich populations and concomitantly decreased known CSC markers. Chrysotoxine suppressed CSC phenotypes through downregulation of Src/protein kinase B (Akt) signaling. Active (phosphorylated Y416) Src was shown to regulate cancer stemness, since ectopic overexpression of Src strongly activated Akt and subsequently enhanced pluripotency transcription factor SRY (sex-determining region Y)-box 2 (Sox2)- mediating CSC phenotypes, whereas the short hairpin RNA of Src and an Src inhibitor (dasatinib) suppressed Akt, Sox2, and CSC properties. Importantly, chrysotoxine was shown to suppress active Src/Akt signaling and in turn depleted Sox2-mediated CSCs. Our findings indicate a novel CSC-targeted role of chrysotoxine and its regulation by Src/Akt and Sox2, which may be exploited for cancer treatment.

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“…The antibiotic ciprofloxacin is found to upregulate Cav-1 in H460 cells and subsequently to impel activated AKT and ERK expressions. Both of them jointly induce the increase in Oct-4 expression, which eventually converts the original cancer cells to CSC-like cells [42]. In addition, culturing human lung epithelial BEAS-2B cells with single-walled carbon nanotubes (SWCNTs) will confer such cells with CSC characteristics.…”

Section: Cav-1-mediated Lung Csc Generationmentioning

confidence: 99%

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

Shi

Lai

et al. 2020

Cancers

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Lung cancer is one of the most common and malignant cancers with extremely high morbidity and mortality in both males and females. Although traditional lung cancer treatments are fast progressing, there are still limitations. Caveolin-1 (Cav-1), a main component of caveolae, participates in multiple cellular events such as immune responses, endocytosis, membrane trafficking, cellular signaling and cancer progression. It has been found tightly associated with lung cancer cell proliferation, migration, apoptosis resistance and drug resistance. In addition to this, multiple bioactive molecules have been confirmed to target Cav-1 to carry on their anti-tumor functions in lung cancers. Cav-1 can also be a predictor for lung cancer patients’ prognosis. In this review, we have summarized the valuable research on Cav-1 and lung cancer in recent years and discussed the multifaceted roles of Cav-1 on lung cancer occurrence, development and therapy, hoping to provide new insights into lung cancer treatment.

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Ciprofloxacin mediates cancer stem cell phenotypes in lung cancer cells through caveolin-1-dependent mechanism

Cited by 25 publications

References 55 publications

Ti_0.8O₂Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

Ti_0.8O₂Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

Cancer Stem Cell–Suppressing Activity of Chrysotoxine, a Bibenzyl fromDendrobium pulchellum

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

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Ciprofloxacin mediates cancer stem cell phenotypes in lung cancer cells through caveolin-1-dependent mechanism

Cited by 25 publications

References 55 publications

Ti0.8O2Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

Ti0.8O2Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

Cancer Stem Cell–Suppressing Activity of Chrysotoxine, a Bibenzyl fromDendrobium pulchellum

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

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Product

Resources

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Ti_0.8O₂Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion

Ti_0.8O₂Nanosheets Inhibit Lung Cancer Stem Cells by Inducing Production of Superoxide Anion