Flavonoids have been proposed as potential chemotherapeutic agents because they are toxic against cancer cells but not harmful to healthy cells. This systematic review analyzed flavonoid effectiveness in human cancer chemotherapy. Overall, 22 phase II and 1 phase III clinical trials (PubMed, Scopus, and Web of Science) that used flavonoids as a single agent or combined with other therapeutics against hematopoietic/lymphoid or solid cancer published by January 2019 were selected for analysis. Flavopiridol was the most commonly used flavonoid (at a dose of 50‐mg/m2 IV) for all tumor types. Aside from the relatively low rate of complete response (CR) or partial response (PR) with any administration protocol, flavonoids showed higher positive outcomes for hematopoietic and lymphoid tissues (140 patients with CR and 88 with PR among 615 patients in 11 trials) than for solid tumors (4 patients with CR and 21 with PR among 525 patients in 12 trials). However, because of the high variety in administration schedule, more studies are needed to further understand how flavonoids can promote positive outcomes for cancer patients.
Cell invasion and metastasis are involved in clinical failures in cancer treatment, and both events require the acquisition of a migratory behavior by tumor cells. Curcumin is a promising natural product with anti-proliferative activity, but its effects on cell migration are still unclear. We evaluated the effects of curcumin on the proliferation, apoptosis, migration, and cell-cell adhesion of keratinocyte, oral squamous cell carcinoma (OSCC), and fibroblast cell lines, as well as in a xenograft model of OSCC. Curcumin (2 μM) decreased cell proliferation in cell lines with mesenchymal characteristics, while cell death was detected only at 50 μM. We observed that highly migratory cells showed a decrease on migration speed and directionality when treated with 2 or 5 μM of curcumin (50% and 40%, respectively, p < 0.05). Using spheroids, we observed that curcumin dose dependently decreased cell-cell adhesion, especially on tumor-derived spheroids. Also, in a xenograft model with patient-derived OSCC cells, the administration of curcumin decreased tumor growth and aggressiveness when compared with untreated tumors, indicating the potential antitumor effect in oral cancer. These results suggest that lower doses of curcumin can influence several steps involved in tumorigenesis, including migration properties, suggesting a possible use in cancer therapy. Copyright © 2017 John Wiley & Sons, Ltd.
Matrix stiffening is ubiquitous in solid tumors and can direct epithelial-mesenchymal transition (EMT) and cancer cell migration. Stiffened niche can even cause poorly invasive oral squamous cell carcinoma (OSCC) cell lines to acquire a less adherent, more migratory phenotype, but mechanisms and durability of this acquired “mechanical memory” are unclear. Here, we observed that contractility and its downstream signals could underlie memory acquisition; invasive SSC25 cells overexpress myosin II (vs. non-invasive Cal27 cells) consistent with OSCC. However, prolonged exposure of Cal27 cells to a stiff niche or contractile agonists upregulated myosin and EMT markers and enabled them to migrate as fast as SCC25 cells, which persisted even when the niche softened and indicated “memory” of their prior niche. Stiffness-mediated mesenchymal phenotype acquisition required AKT signaling and was also observed in patient samples, whereas phenotype recall on soft substrates required focal adhesion kinase (FAK) activity. Phenotype durability was further observed in transcriptomic differences between pre-conditioned Cal27 cells cultured without or with FAK or AKT antagonists, and such transcriptional differences corresponded to discrepant patient outcomes. These data suggest that mechanical memory, mediated by contractility via distinct kinase signaling, may be necessary for OSCC to disseminate.
The aim of this case series was to evaluate the effects of blue®m mouthwash on oral surgical wounds. Eleven patients underwent bilateral preprosthetic surgery and were instructed to apply the product only to the right side of the surgery. In this way, the right side corresponds to the test side and the left side (place without applying any type of solution) to the control side. After seven days of using the product (3 times a day), the following parameters were evaluated by means of a visual analogue scale: pain, changes in taste, and acceptance by the patient. Then, the level of tissue inflammation was assessed, by the number of pixels, using ImageJ® software. The main results show that the blue®m mouthwash was widely accepted by patients, reducing their pain. The number of inflammation pixels was lower on the test side ( p < 0.05 ), indicating improved healing. It is suggested that blue®m mouthwash positively influences tissue healing reducing pain and the postsurgical inflammatory process; however, randomized clinical trials should be done to prove this clinical observation.
Chlorhexidine is widely used in dentistry to treat various gingival conditions. Its side effects are widely described. Histologically, the gingiva consists of a stratified squamous epithelium, with a predominance of keratinocytes, the latter being fundamental in healing processes. Thus, the objective of this in vitro study was to evaluate the effects of a new product with active oxygen (blue®m) on keratinocytes. Keratinocytes (HACAT) were incubated with different concentrations of blue®m (1, 10 and 100 μl/ml), and another well was used as a control, without the presence of mouthwash. After 24, 48 and 72 hours, cell proliferation was analyzed by CyQUANT®. It was possible to observe that lower concentrations (1 μl/ml) of blue®m increased cell proliferation in HACAT cell lines, while moderate and higher concentrations of mouthwash may present a cytotoxic effect. This is the first in vitro study with showing that human keratinocytes cell line demonstrated greater proliferation rate when exposed to lower concentrations of blue®m mouthwash.
Background: Imidazolium salts (IS), ionic derivatives of neutral imidazoles, have properties that can be adjusted by structural modifications to their cations and anions, which makes this particular class of compounds a promising option for developing biologically active compounds. The anti-tumor effects of the IS 1-n-butyl-3-methylim-and 1-n-hexadecyl-2,3-dimethylimidazolium methanesulfonate (C 16 M 2 ImMeS) on oral squamous cell carcinoma (OSCC) have been studied here.Methods: Oral squamous cell carcinoma cells (CAL27) were incubated with increasing IS doses and then submitted to proliferation (2D), cell death (2D) and spheroid assay (3D). Results:The IS anti-tumor effect was dependent on both its N-alkyl chain length and anion, whereby C 16 MImCl proved to be more effective in combination for inhibiting cell proliferation and cell-cell adhesion, outperforming the methylated C 16 M 2 ImCl derivative and, most importantly, the gold standard-cisplatin. In addition, C 16 MImCl had little effect on keratinocytes and more pronounced effects on more aggressive tumor cells. It also exhibited similar effects on inducing cell death when compared to Cisplatin. This compound spread to a greater area of the tumor sphere and produced an enhanced number of apoptotic and necrotic cells in the tumor cell line, demonstrating only a small rise in the healthy cells. Conclusion:These data indicate that the effect of C 16 MlmCl on OSCC is promising, as it is selective for cancer cells.
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