A novel miR-200c/c-myc negative regulatory feedback loop is essential to the EMT process, CSC biology and drug sensitivity in nasopharyngeal cancer

Yang, Jing; Wu, Si-Pei; Wang, Wenjun; Jin, Z; Miao, Xiaobo; Wu, Yue; Gou, Deming; Liu, Qiu-Zhen; Yao, Kangde

doi:10.1016/j.yexcr.2020.111817

Cited by 23 publications

(15 citation statements)

References 35 publications

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“…In addition to the TGF-β/SMAD pathways, miR-200c can overcome chemoresistance by reducing Cathepsin L that has been regarded as a potential target in cancer treatment [69,70]. Moreover, the miR-200c/cmyc negative regulatory feedback loop is crucial for the EMT process and CSC properties as well as drug sensitivity [71]. Nevertheless, there exists an opposite voice about the role of miR-200.…”

Section: Mirnas Inhibit Emt To Overcome Chemotherapy Resistancementioning

confidence: 99%

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Dong

Zhu

et al. 2021

Exp Hematol Oncol

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Cancer stem cells (CSCs) are a small group of cancer cells, which contribute to tumorigenesis and cancer progression. Cancer cells undergoing epithelial-to-mesenchymal transition (EMT) acquire the chemoresistant ability, which is regarded as an important feature of CSCs. Thus, there emerges an opinion that the generation of CSCs is considered to be driven by EMT. In this complex process, microRNAs (miRNAs) are found to play a key role. In order to overcome the drug resistance, inhibiting EMT as well as CSCs phenotype seem feasible. Thereinto, regulating the EMT- or CSCs-associated miRNAs is a crucial approach. Herein, we conduct this review to elaborate on the complicated interplay between EMT and CSCs in cancer chemoresistance, which is modulated by miRNAs. In addition, we elucidate the therapeutic strategy to overcome drug resistance through targeting EMT and CSCs.

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Section: Mirnas Inhibit Emt To Overcome Chemotherapy Resistancementioning

confidence: 99%

MiRNA-mediated EMT and CSCs in cancer chemoresistance

Dong

Zhu

et al. 2021

Exp Hematol Oncol

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“…MYC protein levels have been inversely correlated with miR-200c expression in nasopharyngeal cancer primary tumors. Specifically, MYC has been shown to directly repress miR-200 in a transcription-dependent fashion [ 231 ]. Furthermore, miR-200c reduces the expression of MYC by binding to its 3’-untranslated region, suggesting the existence of a negative feedback loop between MYC and miR-200c.…”

Section: Myc–the Regulator Of Emt and Metastasismentioning

confidence: 99%

“…Furthermore, miR-200c reduces the expression of MYC by binding to its 3’-untranslated region, suggesting the existence of a negative feedback loop between MYC and miR-200c. The over-expression of MYC interferes with this feedback loop, and the repression of miR-200 results in the induction of EMT, dependent on the up-regulation of ZEB1 and ZEB2 [ 108 , 231 ].…”

Section: Myc–the Regulator Of Emt and Metastasismentioning

confidence: 99%

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Meškytė

Keskas

Ciribilli

2020

IJMS

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The Myc family of oncogenes is deregulated in many types of cancer, and their over-expression is often correlated with poor prognosis. The Myc family members are transcription factors that can coordinate the expression of thousands of genes. Among them, c-Myc (MYC) is the gene most strongly associated with cancer, and it is the focus of this review. It regulates the expression of genes involved in cell proliferation, growth, differentiation, self-renewal, survival, metabolism, protein synthesis, and apoptosis. More recently, novel studies have shown that MYC plays a role not only in tumor initiation and growth but also has a broader spectrum of functions in tumor progression. MYC contributes to angiogenesis, immune evasion, invasion, and migration, which all lead to distant metastasis. Moreover, MYC is able to promote tumor growth and aggressiveness by recruiting stromal and tumor-infiltrating cells. In this review, we will dissect all of these novel functions and their involvement in the crosstalk between tumor and host, which have demonstrated that MYC is undoubtedly the master regulator of the tumor microenvironment. In sum, a better understanding of MYC’s role in the tumor microenvironment and metastasis development is crucial in proposing novel and effective cancer treatment strategies.

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“…88,89 miR-200c formed a negative feedback pathway with C-myc, and low expression of C-myc or increased expression of miR-200c promoted chemoresistance. 74 miR-139-5p targets ZEB1 and thereby regulates EMT, inhibits nasopharyngeal carcinoma cell progression, and promotes chemosensitivity to cisplatin. 75,90 In addition, miRNAs may influence chemotherapeutic sensitivity by regulating cell cycle progression.…”

Section: Pathways By Which Mirnas Influence Chemotherapy Resistance In Npcmentioning

confidence: 99%

“… 73 Overexpression of C-myc activates the EMT program and induces the CSC phenotype, therefore promoting drug sensitivity, while miR-200c can negatively feedback with C-myc and inhibit C-myc function, thus promoting chemoresistance. 74 Moreover, Shao et al showed that overexpression of miR-139-5p reversed the progression of EMT in some nasopharyngeal carcinoma cells and improved the chemosensitivity of HNE1 and HNE1/DDP human nasopharyngeal carcinoma cells. 75 Overexpression of miR-BARTs can potentiate the sensitivity to chemotherapeutic agents in some nasopharyngeal epithelial cells.…”

Section: Non-coding Rnas Involved In Drug Resistance Of Npcmentioning

confidence: 99%

Involvement of Non-Coding RNAs in Chemo- and Radioresistance of Nasopharyngeal Carcinoma

Xiao

2021

CMAR

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A novel miR-200c/c-myc negative regulatory feedback loop is essential to the EMT process, CSC biology and drug sensitivity in nasopharyngeal cancer

Cited by 23 publications

References 35 publications

MiRNA-mediated EMT and CSCs in cancer chemoresistance

MiRNA-mediated EMT and CSCs in cancer chemoresistance

MYC as a Multifaceted Regulator of Tumor Microenvironment Leading to Metastasis

Involvement of Non-Coding RNAs in Chemo- and Radioresistance of Nasopharyngeal Carcinoma

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