Prodigiosin Inhibits Proliferation, Migration, and Invasion of Nasopharyngeal Cancer Cells

Abstract

Background/Aims: Nasopharyngeal carcinoma remains a devastating and difficult disease to treat. This study explores the antineoplastic effect of prodigiosin on nasopharyngeal cancer cells. Methods: Human nasopharyngeal carcinoma CNE2 cells and human normal nasopharyngeal epithelial NP69 cells were obtained and treated with prodigiosin or fluorouracil (5-FU). Colony formation assay was performed to screen for the optimal experimental concentrations of prodigiosin and 5-FU, and MTT assay was used to examine cell proliferative ability. Flow cytometry was used to examine cell cycle distribution, the scratch test was employed to examine cell migration, and Transwell migration assay (Boyden chamber) was used to study cell invasion. Results: The optimal concentrations of prodigiosin and 5-FU for treatment were 4 mg/L and 0.35 mg/L, respectively. Both prodigiosin and 5-FU inhibited tumor cell proliferation. The percentage of cells in G0/G1 phase was higher and the percentage of cells in S phase was lower in the prodigiosin and 5-FU groups than in the untreated groups. Both prodigiosin and 5-FU inhibited tumor cell migration and tumor cell invasion. Conclusions: Our results suggest that prodigiosin can inhibit proliferation, migration, and invasion of nasopharyngeal carcinoma cells.

Selective Cytotoxic Activity of Prodigiosin@halloysite Nanoformulation

“…In opposite, the viability of nonmalignant cells (HSF) did not change in all experimental variants. Considering the fact that prodigiosin can suppress cell proliferation, it is expected that the sensitivity of cancer cells to the inhibitory activity of prodigiosin depends on cell proliferation rates (Liu et al, 2018;Sam and Ghoreishi, 2018;Ji et al, 2019).…”

Structural and functional characterization of β2‐glycoprotein I domain 1 in anti‐melanoma cell migration

“…Several studies have characterized cell migration and proliferation in the progression of tumorigenesis. [12][13][14][15] We showed previously that purified β 2 -GPI inhibits cell migration, proliferation, and angiogenesis in human aortic endothelial cells. [9][10][11] However, the role of natural β 2 -GPI in tumor development remains unknown.…”

“…[9][10][11] It is well established that abnormal cell migration and proliferation are closely related to carcinogenesis. [12][13][14][15] Furthermore, many studies have reported that inhibition of cell migration decreases tumor growth in multiple cancers. [16][17][18] Therefore, it is important to elucidate the cellular basis and molecular mechanisms of β 2 -GPI function in antitumorigenesis.…”

“…We previously showed that β 2 ‐GPI plays an essential role in the suppression of vascular endothelial cell growth, cell migration, and angiogenesis under the regulation of nuclear factor‐kappa B (NF‐кB) signaling and vascular endothelial growth factor (VEGF)‐mediated phosphorylation of VEGFR2, ERK1/2 and Akt pathways . It is well established that abnormal cell migration and proliferation are closely related to carcinogenesis . Furthermore, many studies have reported that inhibition of cell migration decreases tumor growth in multiple cancers .…”

Synthesis, Anticancer Potential and Comprehensive Toxicity Studies of Novel Brominated Derivatives of Bacterial Biopigment Prodigiosin from Serratia marcescens ATCC 27117

“…Although the anticancer potential of PG and other prodigiosins has been demonstrated through various modes of action, such as apoptosis [34], autophagy [15], cell cycle arrest [14], mitochondrial uncoupling [35], and migration inhibition [36], toxicity studies of PG are not readily available in the literature. The nematode Caenorhabditis elegans is a model system with well-known developmental stages [37] that can be utilized in anticancer drug discovery for toxicity, immunity, and pharmacogenetics studies, among others [38], so it represents a fitting model system for PG toxicity and safety research.…”