MiRNA-203 Reduces Nasopharyngeal Carcinoma Radioresistance by Targeting IL8/AKT Signaling

Qu, Jia-Quan; Yi, Hongmei; Xu, Ye; Zhu, Jian; Yi, Hong; Li, Lina; Xiao, Ta; Li, Yuan; Li, Jiaoyang; Wang, Yuan‐Yuan; Feng, Juan; He, Qianyu; Lu, Shanshan; Xiao, Zhi‐Qiang

doi:10.1158/1535-7163.mct-15-0461

Cited by 75 publications

(59 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Among these proteins, MIP3α and IL8 are known to enhance the epithelial-to-mesenchymal transition of hepatocellular carcinoma and sustain nasopharyngeal carcinoma radioresistance, respectively. 34,35 Together these other SVZ components could support CXCL12 in mediating GBM resistance to IR in the SVZ environment.…”

Section: Discussionmentioning

confidence: 98%

CXCL12 mediates glioblastoma resistance to radiotherapy in the subventricular zone

et al. 2016

View full text Add to dashboard Cite

). † These authors contributed equally to the present work. AbstractBackground. Patients with glioblastoma (GBM) have an overall median survival of 15 months despite multimodal therapy. These catastrophic survival rates are to be correlated to systematic relapses that might arise from remaining glioblastoma stem cells (GSCs) left behind after surgery. In this line, it has recently been demonstrated that GSCs are able to escape the tumor mass and preferentially colonize the adult subventricular zone (SVZ). At a distance from the initial tumor site, these GSCs might therefore represent a high-quality model of clinical resilience to therapy and cancer relapses as they specifically retain tumor-initiating abilities. Method. While relying on recent findings that have validated the existence of GSCs in the human SVZ, we questioned the role of the SVZ niche as a potential GSC reservoir involved in therapeutic failure.Results. Our results demonstrate that (i) GSCs located in the SVZ are specifically resistant to radiation in vivo, (ii) these cells display enhanced mesenchymal roots that are known to be associated with cancer radioresistance, (iii) these mesenchymal traits are specifically upregulated by CXCL12 (stromal cell-derived factor-1) both in vitro and in the SVZ environment, (iv) the amount of SVZ-released CXCL12 mediates GBM resistance to radiation in vitro, and (v) interferes with the CXCL12/CXCR4 signalling system, allowing weakening of the tumor mesenchymal roots and radiosensitizing SVZ-nested GBM cells. Conclusion. Together, these data provide evidence on how the adult SVZ environment, through the release of CXCL12, supports GBM therapeutic failure and potential tumor relapse. Key wordsCXCL12 | glioblastoma | mesenchymal activation | radioresistance | subventricular zone Primary brain tumors are considered as one of the nastiest scourges faced in oncology. Their most aggressive form, glioblastoma (GBM, WHO grade IV), is also regarded as the most common and lethal subtype. 1 Patients' poor survival rates are typically correlated with unsatisfactory therapeutic strategies leading to systematic GBM relapses. 2 Trying to better

show abstract

Section: Discussionmentioning

confidence: 98%

CXCL12 mediates glioblastoma resistance to radiotherapy in the subventricular zone

et al. 2016

View full text Add to dashboard Cite

show abstract

“…The miR-203 inhibited by EBV-LMP1 targets IL-8, which is a chemotaxis cytokine and immune response mediator (Yu et al, 2011;Yu et al, 2012;Qu et al, 2015). EBVinduced miR-155 and miR-146a are also important molecules in the regulation of the inflammatory reaction (Zhang et al, 2015a;Yang et al, 2016;Bitar et al, 2017).…”

Section: Ebv Regulates the Inflammatory Tumor Microenvironment Via MImentioning

confidence: 99%

An update: Epstein-Barr virus and immune evasion via microRNA regulation

Zuo

Yue

et al. 2017

Virol. Sin.

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) is an oncogenic virus that ubiquitously establishes life-long persistence in humans.To ensure its survival and maintain its B cell transformation function, EBV has developed powerful strategies to evade host immune responses. Emerging evidence has shown that microRNAs (miRNAs) are powerful regulators of the maintenance of cellular homeostasis. In this review, we summarize current progress on how EBV utilizes miRNAs for immune evasion. EBV encodes miRNAs targeting both viral and host genes involved in the immune response. The miRNAs are found in two gene clusters, and recent studies have demonstrated that lack of these clusters increases the CD4 + and CD8 + T cell response of infected cells. These reports strongly indicate that EBV miRNAs are critical for immune evasion. In addition, EBV is able to dysregulate the expression of a variety of host miRNAs, which influence multiple immune-related molecules and signaling pathways. The transport via exosomes of EBV-regulated miRNAs and viral proteins contributes to the construction and modification of the inflammatory tumor microenvironment. During EBV immune evasion, viral proteins, immune cells, chemokines, pro-inflammatory cytokines, and pro-apoptosis molecules are involved. Our increasing knowledge of the role of miRNAs in immune evasion will improve the understanding of EBV persistence and help to develop new treatments for EBV-associated cancers and other diseases.

show abstract

“…In these cells, miR-205 downregulation determined radioresistance by targeting of PTEN [12], miR-451 increases radiosensitivity by targeting RAB14 (RAS related protein 14) [5], miR-23a is associated with modulation of radioresistance by targeting IL8 [13], and miR-185-3p regulates radioresistance, similar to miR-324-3p, by targeting WNT2B [23]. Low expression of miR-203 has been found to be correlated with local disease recurrence after radiotherapy in a series of patients with laryngeal cancer [27] whereas, in NPC, miR-203 plays important role in radiosensitivity by targeting IL8/AKT [28]. On the other hand, downregulation of miR-21 enhances radiosensitivity, but the responsible mechanism has to be clarified in NPC.…”

Section: Involvement Of Mirnas In Radioresistance Of Head and Neckmentioning

confidence: 99%

MicroRNAs Involvement in Radioresistance of Head and Neck Cancer

et al. 2017

View full text Add to dashboard Cite

Resistance to the ionizing radiation is a current problem in the treatment and clinical management of various cancers including head and neck cancer. There are several biological and molecular mechanisms described to be responsible for resistance of the tumors to radiotherapy. Among them, the main mechanisms include alterations in intracellular pathways involved in DNA damage and repair, apoptosis, proliferation, and angiogenesis. It has been found that regulation of these complex processes is often controlled by microRNAs. MicroRNAs are short endogenous RNA molecules that posttranscriptionally modulate gene expression and their deregulated expression has been observed in many tumors including head and neck cancer. Specific expression patterns of microRNAs have also been shown to predict prognosis and therapeutic response in head and neck cancer. Therefore, microRNAs present promising biomarkers and therapeutic targets that might overcome resistance to radiation and improve prognosis of head and neck cancer patients. In this review, we summarize the current knowledge of the functional role of microRNAs in radioresistance of cancer with special focus on head and neck cancer.

show abstract

MiRNA-203 Reduces Nasopharyngeal Carcinoma Radioresistance by Targeting IL8/AKT Signaling

Cited by 75 publications

References 49 publications

CXCL12 mediates glioblastoma resistance to radiotherapy in the subventricular zone

CXCL12 mediates glioblastoma resistance to radiotherapy in the subventricular zone

An update: Epstein-Barr virus and immune evasion via microRNA regulation

MicroRNAs Involvement in Radioresistance of Head and Neck Cancer

Contact Info

Product

Resources

About