MicroRNA-324-3p regulates nasopharyngeal carcinoma radioresistance by directly targeting WNT2B

Li, Guo; Liu, Yong; Su, Zhi; Ren, Shuling; Zhu, Guanghao; Tian, Yongquan; Qiu, Yuanzheng

doi:10.1016/j.ejca.2013.03.001

Cited by 106 publications

(118 citation statements)

References 33 publications

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“…8,9 The present study investigated the roles of miR320a in the proliferation of lung cancer cells, and found that overexpression of miR-320a enhanced the apoptosis of lung adenocarcinoma cells induced by irradiation in vitro and in vivo. Moreover, miR-320a significantly inhibited lung adenocarcinoma cell proliferation and migration by directly regulating STAT3 signals, which was supported by zhao et al, who found that miR-320a plays a critical role in invasion and metastasis of colorectal cancer by regulating Rac1 gene.…”

Section: Discussionmentioning

confidence: 99%

“…7 Qu et al showed that miR-205 contributes to the radioresistance of nasopharyngeal carcinoma by directly targeting phosphatase and tensin homolog deleted on chromosome 10. 8 A recent report demonstrated that the radioresistance of lung adenocarcinoma is linked to dysregulated miR-451/c-Myc-survivin/rad-51 signaling. Furthermore, miR-451 can promote radioresistance of cancer cell apoptosis by directly targeting c-Myc.…”

Section: Introductionmentioning

confidence: 99%

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MiR-320a effectively suppresses lung adenocarcinoma cell proliferation and metastasis by regulating STAT3 signals

et al. 2017

Cancer Biology & Therapy

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MicroRNAs play important roles in tumorigenesis of various types of cancers. MiR-320a can inhibits cell proliferation of some cancers, but the biologic roles of miR-320a in lung cancer need to be further studied. Here, we investigated the roles of miR-320a in suppressing the proliferation of lung adenocarcinoma cells. MiR-320a treatment was found to effectively suppress LTEP-a-2 and A549 cell proliferation, and induce more apoptotic cells with irradiation treatment compared with control treatment. Our results also showed that miR-320a, as a novel miRNA, directly regulated signal transducer and activator of transcription 3 (STAT3) and its signals, such as Bcl ¡ 2, Bax, and Caspase 3. The siRNA-inhibited STAT3 levels further proved its roles in regulating STAT3 signals. Moreover, miR-320a treatment effectively suppressed cancer cell growth in mice xenografts compared with controls, and significantly inhibited cell migration in vitro and in vivo. Our findings collectively demonstrated that miR-320a, by directly regulating STAT3 signals, not only suppressed cell proliferation and metastasis, but also enhanced irradiation-induced apoptosis of adenocarcinomia cells.Abbreviations: GFP, green fluorescent protein; HE, hematoxylin-eosin staining; miRNAs, microRNAs; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NSCLC, Non-small cell lung cancer; STAT3, signal transducer and activator of transcription 3

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiR-320a effectively suppresses lung adenocarcinoma cell proliferation and metastasis by regulating STAT3 signals

et al. 2017

Cancer Biology & Therapy

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“…Over the past few years, several miRs involving in tumor radioresistance such as miR-21 (9), miR-95 (10), miR-23b (11), let7 (12), miR-205 (13), miR-210 (14), miR-181a (15), miR-125b (16), and miR-324-3p (17) have been identified.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2015

Molecular Cancer Therapeutics

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Radioresistance poses a major challenge in nasopharyngeal carcinoma (NPC) treatment, but little is known about how miRNA (miR) regulates this phenomenon. In this study, we investigated the function and mechanism of miR-203 in NPC radioresistance, one of downregulated miRs in the radioresistant NPC cells identified by our previous microarray analysis. We observed that miR-203 was frequently downregulated in the radioresistant NPC tissues compared with radiosensitive NPC tissues, and its decrement significantly correlated with NPC radioresistance and poor patient survival, and was an independent predictor for reduced patient survival. In vitro radioresponse assays showed that miR-203 mimic markedly decreased NPC cell radioresistance. In a mouse model, therapeutic administration of miR-203 agomir dramatically sensitized NPC xenografts to irradiation. Mechanistically, we confirmed that IL8 was a direct target of miR-203, and found that reduced miR-203 promoted NPC cell radioresistance by activating IL8/ AKT signaling. Moreover, the levels of IL8 and phospho-AKT were significantly increased in the radioresistant NPC tissues compared with radiosensitive NPC tissues, and negatively associated with miR-203 level. Our data demonstrate that miR-203 is a critical determinant of NPC radioresponse, and its decrement enhances NPC radioresistance through targeting IL8/AKT signaling, highlighting the therapeutic potential of the miR-203/IL8/AKT signaling axis in NPC radiosensitization. Mol Cancer Ther; 14(11); 2653-64. Ó2015 AACR.

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“…In the present study, it was observed that hsa-miR-185-5p was significantly dysregulated in chordoma tissues and had the potential to target the Wnt signaling pathway. Li et al (22) confirmed that miR-185-3p contributed to the radioresistance of nasopharyngeal carcinoma via modulation of WNT2B expression in vitro. Liu et al (23) confirmed that miR-185 was a negative regulator of RhoA and cell division cycle 42, and their cellular activities, and was able to inhibit proliferation and invasion of colorectal cancer cells.…”

Section: Discussionmentioning

confidence: 65%

MicroRNA profiling and bioinformatics analyses reveal the potential roles of microRNAs in chordoma

Chen

Zhang

et al. 2017

Oncol Lett

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Abstract. Chordoma is a rare aggressive bone tumor arising from remnants of the notochord, and patients with chordoma have a poor prognosis. However, the unique expression profiles of microRNAs (miRNAs/miRs) and their downstream signaling pathways in chordoma remain incompletely characterized. The aim of the present study was to delineate the global miRNA expression profile and associated signaling networks in chordoma. miRNA profiling was performed on chordoma and fetal notochord tissues. Differentially expressed miRNAs in chordoma were analyzed using microarrays with hierarchical clustering analysis. The target genes of the differentially expressed miRNAs were predicted, and Gene Ontology (GO) and pathway analyses were performed for the intersecting genes. A total of 42 miRNAs were significantly dysregulated in chordoma compared with that in fetal nucleus pulposus tissues. The expression of hsa-miR-21-3p, hsa-miR-150-5p, hsa-miR-1290 and hsa-miR-623 were validated using the reverse transcription-quantitative polymerase chain reaction. On the basis of the intersection predicted by three databases (Targetscan, microRNA.org and PITA), 10,292 potential miRNA targets were identified. Bioinformatic analyses suggested that these dysregulated miRNAs and their predicted targets were functions of signaling pathways in cancer, the mitogen-activated protein kinase signaling pathway, regulation of actin cytoskeleton, focal adhesion and endocytosis. In particular, human (hsa-)miR-185-5p was identified as a crucial miRNA in chordoma development via the Wnt signaling pathway. The results of the present study provide a comprehensive expression and functional profile of differentially expressed miRNAs associated with chordoma. This profile may serve as a potential tool for biomarker and therapeutic target identification in patients with chordoma.

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MicroRNA-324-3p regulates nasopharyngeal carcinoma radioresistance by directly targeting WNT2B

Cited by 106 publications

References 33 publications

MiR-320a effectively suppresses lung adenocarcinoma cell proliferation and metastasis by regulating STAT3 signals

MiR-320a effectively suppresses lung adenocarcinoma cell proliferation and metastasis by regulating STAT3 signals

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

MicroRNA profiling and bioinformatics analyses reveal the potential roles of microRNAs in chordoma

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