Antrodia cinnamomea mycelial fermentation broth inhibits the epithelial-mesenchymal transition of human esophageal adenocarcinoma cancer cells

Liu, Yu Ming; Liu, Yu Kuo; Huang, Pin I.; Tsai, Tung Hu; Chen, Yu-Jen

doi:10.1016/j.fct.2018.01.028

Cited by 9 publications

(9 citation statements)

References 35 publications

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“…A critical feature of these cancer cells has the ability to disintegrate the extracellular matrix (ECM) and basement membranes, largely mediated by matrix metalloproteinases (MMPs) [32]. Previous studies also have shown AC plays an important role in anti-inflammatory and anti-cancer in different cancers and animal models [19,33]. Our results also determine that AC mediated anti-cancer effects in CRC’s were associated with the decreased expression of EMT related β-catenin and vimentin genes (Figure 4A).…”

Section: Resultsmentioning

confidence: 99%

“…Recent studies also indicate that AC not only causing the apoptosis to tumor cell, but also protects liver cells from free radical-induced oxidative stress through the Nrf-2 activation and up-regulation of the MAP kinase-mediated antioxidant genes [14,15]. Furthermore, AC inhibits the proliferation of head and neck cancer cells and migration of leukaemia cells [16,17,18,19]. These findings strongly suggest AC can be a potential source of new cancer therapeutics.…”

Section: Introductionmentioning

confidence: 99%

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Antrodia cinnamomea Enhances Chemo-Sensitivity of 5-FU and Suppresses Colon Tumorigenesis and Cancer Stemness via Up-Regulation of Tumor Suppressor miR-142-3p

et al. 2019

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5-Fluorouracil (5-FU) regimen remains the backbone of the first-line agent to treat colon cancer, but often these patients develop resistance. Cancer stem cells (CSC’s) are considered as one of the key contributors in the development of drug resistance and tumor recurrence. We aimed to provide preclinical evidence for Antrodia cinnamomea (AC), as a potential in suppressing colon cancer CSC’s to overcome 5-FU drug-resistant. In-vitro assays including cell viability, colony formation, AC + 5-FU drug combination index and tumor sphere generation were applied to determine the inhibitory effect of AC. Mouse xenograft models also incorporated to evaluate in vivo effect of AC. AC treatment significantly inhibited the proliferation, colony formation and tumor sphere generation. AC also inhibited the expression of oncogenic markers (NF-κB, and C-myc), EMT/metastasis markers (vimentin and MMP3) and stemness associated markers (β-catenin, SOX-2 and Nanog). Sequential treatment of AC and 5-FU synergized and reduces colon cancer viability both in vivo and in vitro. Mechanistically, AC mediated anti-tumor effect was associated with an increased level of tumor suppressor microRNAs especially, miR142-3p. AC can be a potent synergistic adjuvant, down-regulates cancer stemness genes and enhances the antitumor ability of 5-FU by stimulating apoptosis-associated genes, suppressing inflammation and metastasis genes through miR142-3p in colon cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Antrodia cinnamomea Enhances Chemo-Sensitivity of 5-FU and Suppresses Colon Tumorigenesis and Cancer Stemness via Up-Regulation of Tumor Suppressor miR-142-3p

et al. 2019

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“…Among them, the antimetastatic properties of A. cinnamomea are of particular interest. Recent studies have demonstrated that crude extracts or pure compounds have the ability of inhibit cancer cell metastasis via modulation of the EMT process [17,[20][21][22]. The anti-cancer properties of A. cinnamomea have been attributed to its unique composition of phytochemicals such as antroquinonols, antcins, and antrodins [12-15, 23, 24].…”

Section: Discussionmentioning

confidence: 99%

Antcin-A Modulates Epithelial-to-Mesenchymal Transition and Inhibits Migratory and Invasive Potentials of Human Breast Cancer Cells via p53-Mediated miR-200c Activation

et al. 2019

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Antcin-A (ATA) is a steroid-like phytochemical isolated from the fruiting bodies of a precious edible mushroom Antrodia cinnamomea. We previously showed that ATA has strong anti-inflammatory and anti-tumor effects; however, other possible bioactivities of this unique compound remain unexplored. In the present study, we aimed to investigate the modulation of epithelial-to-mesenchymal transition (EMT), anti-migration, and anti-invasive potential of ATA against human breast cancer cells in vitro. Human breast cancer cell lines, MCF-7 and MDA-MB-231, were incubated with ATA for 24 h. Wound healing, trans-well invasion, western blot, q-PCR, F-actin staining, and immunofluorescence assays were performed. We found that treatment with ATA significantly blocked EMT processes, as evidenced by upregulation of epithelial markers (E-cadherin and occludin) and downregulation of mesenchymal markers (N-cadherin and vimentin) via suppression of their transcriptional repressor ZEB1. Next, we found that ATA could induce miR-200c, which is a known player of ZEB1 repression. Further investigations revealed that ATA-mediated induction of miR-200c is associated with transcriptional activation of p53, as confirmed by the fact that ATA failed to induce miR-200c or suppress ZEB1 activity in p53 inhibited cells. Further in vitro wound healing and trans-well invasion assays support that ATA could inhibit migratory and invasive potentials of breast cancer cells, and the effect was likely associated with induced phenotypic modulation. Taken together, the present study suggests that antcin-A could be a lead phyto-agent for the development of anti-metastatic drug for breast cancer treatment.

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“…Liu et al (59) demonstrated that Antrodia cinnamomea mycelial fermentation broth blocked the cell cycle progression of EC cells in the G 2 /M phase by upregulating the expression of p21, thus rendering the cells more sensitive to the subsequent dose of radiation. The aforementioned simple examples demonstrate that p21-regulated drugs have exhibited potent antitumor effects in experiments; a number of other studies have also proven this effect (58,(60)(61)(62)(63)(64)(65)(66)(67).…”

Section: Role Of P21 In the Treatment Of Esophageal Cancermentioning

confidence: 99%

Function of p21 and its therapeutic effects in esophageal cancer (Review)

et al. 2020

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Esophageal cancer (EC) is the eighth most common type of cancer worldwide and ranks sixth among the causes of cancer-related mortality. Due to the high mortality rate and poor treatment efficacy for EC, millions of individuals succumb to this disease; thus, the identification of novel treatment targets is of utmost importance and urgency. In recent years, there have been advances if therapies targeting cell cycle regulators. p21 is a type of cell cycle regulator that plays a dual role in tumor cells, as it can not only regulate the cell cycle, induce apoptosis and inhibit cell proliferation, but can also protect cells from apoptosis. It has been found that p21 often exerts a tumor-suppressive effect on EC, which provides a basis for its use as a treatment target for EC. Therefore, the aim of the present study was to review the function of p21 and its potential value as a therapeutic target for EC.

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Antrodia cinnamomea mycelial fermentation broth inhibits the epithelial-mesenchymal transition of human esophageal adenocarcinoma cancer cells

Cited by 9 publications

References 35 publications

Antrodia cinnamomea Enhances Chemo-Sensitivity of 5-FU and Suppresses Colon Tumorigenesis and Cancer Stemness via Up-Regulation of Tumor Suppressor miR-142-3p

Antrodia cinnamomea Enhances Chemo-Sensitivity of 5-FU and Suppresses Colon Tumorigenesis and Cancer Stemness via Up-Regulation of Tumor Suppressor miR-142-3p

Antcin-A Modulates Epithelial-to-Mesenchymal Transition and Inhibits Migratory and Invasive Potentials of Human Breast Cancer Cells via p53-Mediated miR-200c Activation

Function of p21 and its therapeutic effects in esophageal cancer (Review)

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