The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma

Jin, Chuan; Yan, Bingchuan; Lu, Qin; Lin, Yanmin; Ma, Lei

doi:10.1007/s13277-015-4227-z

Cited by 97 publications

(100 citation statements)

References 25 publications

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“…Conversely, knockdown of MALAT1 could sensitize NPC cells to radiation both in vitro and in vivo . Furthermore, there was reciprocal repression between MALAT1 and miR-1, MALAT1 regulated radioresistance by modulating cancer stem cell (CSC) activity through regulating miR-1/slug axis [93]. The above studies suggested that MALAT1 could act as a therapeutic target for NPC patients.…”

Section: Oncogenic Lncrnasmentioning

confidence: 99%

Functions and Roles of Long-Non-Coding RNAs in Human Nasopharyngeal Carcinoma

Hann²

2018

Cell Physiol Biochem

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Nasopharyngeal carcinoma (NPC) is one of the most common cancers originating in the nasopharynx and occurring at high frequency in South-eastern Asia and North Africa. Long non-coding RNAs (lncRNAs) are a class of non-protein-coding RNA molecules and key regulators of developmental, physiological, and pathological processes in humans. Emerging studies have shown that lncRNAs play critical roles in tumorgenicity and cancer prognosis. With the development of deep sequencing analyses, an extensive amount of functional lncRNAs have been discovered in nasopharyngeal carcinoma tissues and cell lines. However, the roles and mechanisms of aberrantly expressed lncRNAs in the pathogenesis of NPC are not fully understood. In this review, we briefly illustrate the concept, identification, functional characterization, and summarize recent advancements of biological functions of lncRNAs with heterogeneous mechanistic characterization and their involvement in NPC. Then, we describe individual lncRNAs that have been associated with tumorgenesis, growth, invasion, cancer stem cell differentiation, metastasis, drug resistance and discuss the strategies of their therapeutic manipulation in NPC. We also review the emerging insights into the role of lncRNAs and their potential as biomarkers and therapeutic targets for novel treatment paradigms. Finally, we highlight the up-to-date of clinical information involving lncRNAs and future directions in the linking lncRNAs to potential gene therapies, and how modifications of lncRNAs can be exploited for prevention and treatment of NPC.

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Section: Oncogenic Lncrnasmentioning

confidence: 99%

Functions and Roles of Long-Non-Coding RNAs in Human Nasopharyngeal Carcinoma

Hann²

2018

Cell Physiol Biochem

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“…In melanoma cells, miR-9 overexpression induced downregulation of Snail with a concomitant increased EMT phenotype via translational repression of NF κ B [90]. miR-1 downregulates Slug and such regulation has been functionally linked to EMT, CSC activity, and radio-resistance [57, 91]. Additionally, miR-124, miR-204, and miR-211 have been shown to directly inhibit Slug and revert mesenchymal (or promote epithelial) phenotype in various cell lines [92–95].…”

Section: Translational Control Of Emt-tfsmentioning

confidence: 99%

Tackling Cancer Stem Cells via Inhibition of EMT Transcription Factors

Mladinich

Ruan

Chan

2016

Stem Cells International

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Cancer stem cell (CSC) has become recognized for its role in both tumorigenesis and poor patient prognosis in recent years. Traditional therapeutics are unable to effectively eliminate this group of cells from the bulk population of cancer cells, allowing CSCs to persist posttreatment and thus propagate into secondary tumors. The therapeutic potential of eliminating CSCs, to decrease tumor relapse, has created a demand for identifying mechanisms that directly target and eliminate cancer stem cells. Molecular profiling has shown that cancer cells and tumors that exhibit the CSC phenotype also express genes associated with the epithelial-to-mesenchymal transition (EMT) feature. Ample evidence has demonstrated that upregulation of master transcription factors (TFs) accounting for the EMT process such as Snail/Slug and Twist can reprogram cancer cells from differentiated to stem-like status. Despite being appealing therapeutic targets for tackling CSCs, pharmacological approaches that directly target EMT-TFs remain impossible. In this review, we will summarize recent advances in the regulation of Snail/Slug and Twist at transcriptional, translational, and posttranslational levels and discuss the clinical implication and application for EMT blockade as a promising strategy for CSC targeting.

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“…Several genes have been suggested to be involved in radioresistance in NPC, such as integrin, MiR-205, MiR-203, RKIP, MALAT1, 14-3-3σ, Maspin, RKIP, and GRP78. [20][21][22][23][27][28][29][30][31] Though proteomics examination of the differently expressed proteins in radioresistant cell line and its parental cell line CNE-2, Feng et al 32 identified 34 differential proteins. In this study, we found the expression of EMP2 was almost lost in CNE-2, and its re-expression significantly promoted cell apoptosis when combined with radiation treatment.…”

Section: Discussionmentioning

confidence: 99%

EMP2 re-expression inhibits growth and enhances radiosensitivity in nasopharyngeal carcinoma

et al. 2017

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Although radiation therapy is the primary treatment for nasopharyngeal carcinoma, radioresistance remains a major obstacle to successful treatment in many cases, and the exact underlying molecular mechanisms are still ill-defined. EMP2, epithelial membrane protein-2, was a recently identified potential oncogene involved in multiple biological processes including cell migration and cell proliferation. This study was to explore the potential relationship between EMP2 expression, nasopharyngeal carcinoma genesis, and radioresistance. EMP2 expression status in 98 nasopharyngeal carcinoma clinical samples was examined by immunohistochemical staining. As a result, most of the nasopharyngeal carcinoma tumor samples were weakly or negatively stained, while paired adjacent normal tissues were moderately or strongly stained. Moreover, patients with higher expression of EMP2 had significant longer survival times. EMP2 re-expression suppresses cell growth, induces S-phase cell cycle arrest, and promotes radiosensitivity and apoptosis in nasopharyngeal carcinoma cells. These results support that loss of EMP2 is common, and its re-expression may serve as an approach to enhance radiation sensitivity in nasopharyngeal carcinoma.

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The role of MALAT1/miR-1/slug axis on radioresistance in nasopharyngeal carcinoma

Cited by 97 publications

References 25 publications

Functions and Roles of Long-Non-Coding RNAs in Human Nasopharyngeal Carcinoma

Functions and Roles of Long-Non-Coding RNAs in Human Nasopharyngeal Carcinoma

Tackling Cancer Stem Cells via Inhibition of EMT Transcription Factors

EMP2 re-expression inhibits growth and enhances radiosensitivity in nasopharyngeal carcinoma

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