The inhibition of cordycepin on cancer stemness in TGF-beta induced chemo-resistant ovarian cancer cell

Wang, Chia Woei; Lee, Bao Hong; Tai, Chen Jei

doi:10.18632/oncotarget.22951

Cited by 13 publications

(14 citation statements)

References 26 publications

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“…Cordycepin efficiently inhibited cell viability, the percentage of ovarian cancer stem cells, and the levels of matrix metalloproteinases (MMPs) in TGF-beta-induced SKOV-3 ovarian cancer cells. Thus, cordycepin acted as a complementary agent for ovarian cancer therapy that against chemoresistance (Wang et al, 2017c).…”

Section: Cordycepin Inhibits Tumor Growthmentioning

confidence: 99%

“…Cordycepin can suppress mitochondrial fusion-induced EMT in ovarian carcinoma cells through inhibiting estrogen-related receptor (ERR)-α, which is a co-transcription factor for gene expressions associated with mitochondrial fusion Thus, cordycepin suppresses metastasis and migration of ovarian carcinoma cells via inhibiting mitochondrial activity (Wang et al, 2017b). In addition, Cordycepin also blocked EMT through regulating TGF-β (Wang et al, 2017c).…”

Section: Regulation Of Cordycepin On Tumor Microenvironmentmentioning

confidence: 99%

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Anti-tumor and anti-metastatic roles of cordycepin, one bioactive compound of Cordyceps militaris

Jin

Meng

Qiu

et al. 2018

Saudi Journal of Biological Sciences

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Public interest in complementary and alternative medicine has been increased worldwide, due to its wide applications in cancer prevention and treatment. Cordycepin is one of the most common and crucial types of complementary and alternative medicine. Cordycepin (3'-deoxyadenosine), a derivative of adenosine, was first isolated from medicine drug . Cordycepin has been widely used as one compound for antitumor, which has been found to exert antiangiogenic, anti-metastatic, and antiproliferative effects, as well as inducing apoptosis. However, the mechanism of its anti-tumor activity is not well known. This review will clarify anti-tumor mechanisms of Cordycepin, which regulate signaling pathways related with tumor growth and metastasis. Cordycepin inhibit tumor growth via upregulating tumor apoptosis, inducing cell cycle arrest and targeting cancer stem cells (CSCs). Cordycepin regulates tumor microenvironment via suppressing tumor metastasis-related pathways. Thus, Cordycepins may be one of important supplement or substitute medicine drug for cancer treatment.

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Section: Cordycepin Inhibits Tumor Growthmentioning

confidence: 99%

Section: Regulation Of Cordycepin On Tumor Microenvironmentmentioning

confidence: 99%

Anti-tumor and anti-metastatic roles of cordycepin, one bioactive compound of Cordyceps militaris

Jin

Meng

Qiu

et al. 2018

Saudi Journal of Biological Sciences

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“…Although the role of cordycepin on ABC transporters to treat multidrug-resistant tumors has not been investigated in much detail, there are several studies emphasizing that cordycepin can re-sensitize tumors to DNA-damaging chemotherapeutics such as cisplatin, temozolomide, doxorubicin and also radiotherapy. [56][57][58][59][60][61][62][63][64][65][66] Still, limited number of investigations mentioned cordycepin's effects on ABC transporters. To exemplify, a notable P-gp inhibitory property of cordycepin has been uncovered through the stimulation of P-gp ATPase activity, 47 which may form a rationale basis for our assumptions.…”

Section: Classical Mechanisms Of Drug Resistancementioning

confidence: 99%

Activity of Cordycepin From Cordyceps sinensis Against Drug-Resistant Tumor Cells as Determined by Gene Expression and Drug Sensitivity Profiling

Özenver

Boulos

Efferth

2021

Natural Product Communications

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Cordycepin is one of the substantial components of the parasitic fungus Cordyceps sinensis as well as other Cordyceps species. It exerts various effects such as antimetastatic, antiinflammatory, antioxidant, and neuroprotective activities. Assorted studies revealed in vitro and in vivo anticancer influence of cordycepin and put forward its potential for cancer therapy. However, the role of multidrug resistance-associated mechanisms for the antitumor effect of cordycepin has not been investigated in great detail thus far. Therefore, we searched cordycepin’s cytotoxicity with regard to well-known anticancer drug resistance mechanisms, including ABCB1, ABCB5, ABCC1, ABCG2, EGFR, and TP53, and identified putative molecular determinants related to the cellular responsiveness of cordycepin. Bioinformatic analyses of NCI microarray data and gene promoter transcription factor binding motif analyses were performed to specify the mechanisms of cordycepin towards cancer cells. COMPARE and hierarchical analyses led to the detection of the genes involved in cordycepin’s cytotoxicity and sensitivity and resistance of cell lines towards cordycepin. Tumor-type dependent response and cross-resistance profiles were further unravelled. We found transcription factors potentially involved in the common transcriptional regulation of the genes identified by COMPARE analyses. Cordycepin bypassed resistance mediated by the expression of ATP-binding cassete (ABC) transporters (P-gp, ABCB5, ABCC1 and BCRP) and mutant epidermal growth factor receptor (EGFR). The drug sensitivity profiles of several DNA Topo I and II inhibitors were significantly correlated with those of cordycepin’s activity. Among eight different tumor types, prostate cancer was the most sensitive, whereas renal carcinoma was the most resistant to cordycepin. NF-κB was discovered as a common transcription factor. The potential of cordycepin is set forth as a potential new drug lead by bioinformatic evaluations. Further experimental studies are warranted for better understanding of cordycepin’s activity against cancer.

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“…Cordycepin from the fungus Cordyceps militaris can suppress LPS-induced cytokine production by increasing heme oxygenase-1 expression [135,136]. Cordycepin (25-100 µM) can inhibit cancer stemness of TGF-induced chemo-resistant ovarian cancer cells [137]. Metronomic cordycepin therapy (25 mg/kg and 50 mg/kg) can prolong the survival of oral cancer-bearing mice and it (50 µM) inhibit EMT [138].…”

Section: Reversal Of Emt By Anti-inflammatory Natural Compoundsmentioning

confidence: 99%

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Lee

2019

Cancers

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Epithelial mesenchymal transition (EMT) is a key process in the progression of malignant cancer. Therefore, blocking the EMT can be a critical fast track for the development of anticancer drugs. In this paper, we update recent research output of EMT and we explore suppression of EMT by natural anti-inflammatory compounds and pro-resolving lipids.A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the m ajor signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2) belongs to the runt-related transcription factor family [19]. Runx2 plays a key role in EMT of hepatocellular carcinoma (HCC) [20]. GATA transcription factors are also implicated in the EMT of cancer cells [21].A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the major signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2...

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The inhibition of cordycepin on cancer stemness in TGF-beta induced chemo-resistant ovarian cancer cell

Cited by 13 publications

References 26 publications

Anti-tumor and anti-metastatic roles of cordycepin, one bioactive compound of Cordyceps militaris

Anti-tumor and anti-metastatic roles of cordycepin, one bioactive compound of Cordyceps militaris

Activity of Cordycepin From Cordyceps sinensis Against Drug-Resistant Tumor Cells as Determined by Gene Expression and Drug Sensitivity Profiling

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

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