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The Antitumor Effect of Caffeic Acid Phenethyl Ester by Downregulating Mucosa-Associated Lymphoid Tissue 1 via AR/p53/NF-κB Signaling in Prostate Carcinoma Cells.

ABSTRACT: Caffeic acid phenethyl ester (CAPE), a honeybee propolis-derived bioactive ingredient, has not been extensively elucidated regarding its effect on prostate cancer and associated mechanisms. The mucosa-associated lymphoid tissue 1 gene (MALT1) modulates NF-κB signal transduction in lymphoma and non-lymphoma cells. We investigated the functions and regulatory mechanisms of CAPE in relation to MALT1 in prostate carcinoma cells. In p53- and androgen receptor (AR)-positive prostate carcinoma cells, CAPE downregulated AR and MALT1 expression but enhanced that of p53, thus decreasing androgen-induced activation of MALT1 and prostate-specific antigen expressions. p53 downregulated the expression of MALT in prostate carcinoma cells through the putative consensus and nonconsensus p53 response elements. CAPE downregulated MALT1 expression and thus inhibited NF-κB activity in p53- and AR-negative prostate carcinoma PC-3 cells, eventually reducing cell proliferation, invasion, and tumor growth in vitro and in vivo. CAPE induced the ERK/JNK/p38/AMPKα1/2 signaling pathways; however, pretreatment with the corresponding inhibitors of MAPK or AMPK1/2 did not inhibit the CAPE effect on MALT1 blocking in PC-3 cells. Our findings verify that CAPE is an effective antitumor agent for human androgen-dependent and -independent prostate carcinoma cells in vitro and in vivo through the inhibition of MALT1 expression via the AR/p53/NF-κB signaling pathways.

SUBMITTER: Chang KS

PROVIDER: S-EPMC8773797 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature

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The Antitumor Effect of Caffeic Acid Phenethyl Ester by Downregulating Mucosa-Associated Lymphoid Tissue 1 via AR/p53/NF-κB Signaling in Prostate Carcinoma Cells.

Chang Kang-Shuo KS Tsui Ke-Hung KH Hsu Shu-Yuan SY Sung Hsin-Ching HC Lin Yu-Hsiang YH Hou Chen-Pang CP Yang Pei-Shan PS Chen Chien-Lun CL Feng Tsui-Hsia TH Juang Horng-Heng HH

Cancers 20220106 2

Caffeic acid phenethyl ester (CAPE), a honeybee propolis-derived bioactive ingredient, has not been extensively elucidated regarding its effect on prostate cancer and associated mechanisms. The mucosa-associated lymphoid tissue 1 gene (<i>MALT1</i>) modulates NF-κB signal transduction in lymphoma and non-lymphoma cells. We investigated the functions and regulatory mechanisms of CAPE in relation to <i>MALT1</i> in prostate carcinoma cells. In p53- and androgen receptor (AR)-positive prostate carc ...[more]

PMID: 35053438

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Project description:BackgroundCaffeic acid phenethyl ester (CAPE), a natural phenolic compound, has demonstrated antibacterial effects. Dental caries etiology is multifactorial, including a cariogenic biofilm containing multispecies bacteria. However, the antibacterial property of CAPE on multispecies biofilm is unclear. The aim of this study was to assess the effect of CAPE on the formation and cariogenicity in biofilm containing Streptococcus mutans, Streptococcus oralis, and Streptococcus mitis.MethodsS. mutans (ATCC 25175), S. oralis (ATCC 35037), and S. mitis (ATCC 49456T) were employed in this investigation. Each bacterial strain was cultured in the presence of CAPE, followed by susceptibility assessment through optical density measurements at a 600 nm wavelength. Multispecies biofilm formation was achieved by co-culturing S. mutans, S. oralis, and S. mitis at a 1:1:1 ratio on hydroxyapatite-coated 96-well plates. The anti-adherence activity of CAPE on multispecies biofilm was evaluated using a crystal violet staining assay. Cariogenic gene expression level and glucosyltransferase (GTF) function in CAPE-treated mixed bacteria were evaluated using real-time PCR and enzyme activity assay, respectively. The thickness and bacterial viability in CAPE-treated multispecies biofilm were examined using confocal laser scanning microscopy.ResultsCAPE demonstrated a significant antimicrobial effect on S. mutans, S. oralis, and S. mitis (p < 0.05). The inhibition concentration 50% (IC50) of CAPE against S. mutans, S. oralis, and S. mitis ranged from 1.6-6.4 mg/ml. CAPE significantly hindered the multispecies biofilm adherence (p < 0.05). Furthermore, the expression of genes involved in acidogenicity, aciduricity, sucrose-dependent adhesion and quorum sensing mechanism and GTF activity were significantly decreased in CAPE-treated mixed bacteria (p < 0.05). In a multispecies biofilm, CAPE significantly reduced its thickness and viable bacteria population (p < 0.05). In conclusion, CAPE exhibited antimicrobial, anti-adherence and anti-cariogenic effects within a multispecies biofilm. These findings suggest the potential use of CAPE as an adjunctive anti-cariogenic agent in future dental applications.

Project description:Purpose: Caffeic acid phenethyl ester (CAPE) is the main polyphenol extracted from honeybee propolis, which inhibits the growth of several kinds of tumor. This study aimed to assess the inhibitory effect of CAPE in nasopharyngeal carcinoma (NPC), evaluate the synergistic action of CAPE in radiotherapy sensitivity of NPC cell lines and further elucidate the possible molecular mechanism involved. Materials and methods: CCK-8 assay was used to analyze cell proliferation ability. Colony formation assay was used to evaluate the clonogenic ability and radio-sensitiveness of NPC cells by CAPE treatment. Wound-healing and transwell assay were used to assess the motility of cells. The expression of key molecules of the epithelial-mesenchymal transition (EMT) was determined by western blot analysis and changes in radiation sensitivity were measured by colony-formation assay. cDNA microarray analysis was used to determine differentially expressed genes with and without CAPE treatment, with Gene Ontology enrichment of gene function and KEGG pathways determined. Cell cycle and apoptosis were detected by flow cytometry and western blot analysis. Results: CAPE suppressed the viability of NPC cell lines time- and dose-dependently. It induced apoptosis in NPC cells along with decreased expression of Bcl-XL and increased cleavage of PARP and expression of Bax. G1 phase arrest was induced by CAPE with ower expression of CDK4, CDK6, Rb and p-Rb. The migratory and invasive ability of NPC cells was decreased by the EMT pathway. The irradiation sensitivity of NPC cells was enhanced with CAPE treatment. CAPE specifically inhibited nuclear factor κB (NF-κB) signaling pathway by suppressing p65 subunit translocation from cytoplasm to nucleus. CAPE treatment was synergistic with chemotherapy and radiotherapy. Conclusion: CAPE may inhibit the proliferation and metastasis of NPC cells but enhance radiosensitivity in NPC therapy by inhibiting the NF-κB pathway. CAPE could be a potential therapeutic compound for NPC therapy.

Dataset Information

The Antitumor Effect of Caffeic Acid Phenethyl Ester by Downregulating Mucosa-Associated Lymphoid Tissue 1 via AR/p53/NF-κB Signaling in Prostate Carcinoma Cells.

Publications

The Antitumor Effect of Caffeic Acid Phenethyl Ester by Downregulating Mucosa-Associated Lymphoid Tissue 1 via AR/p53/NF-κB Signaling in Prostate Carcinoma Cells.

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