Update zur kombinierten Radio-, Radiochemo- und alleinigen Chemotherapie bei der multimodalen Therapie des Nasopharynxkarzinoms – eine MAC-NPC-Metaanalyse

Becker-Schiebe, Martina; Christiansen, Hans

doi:10.1007/s00066-015-0904-5

Cited by 7 publications

(5 citation statements)

References 11 publications

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“…Epstein-Barr virus infection, tumor suppressors, oncogenes and environmental factors are associated with the tumorigenesis of NPC, but the molecular mechanism of its pathogenesis remains to be completely clarified [3]. Though enhanced susceptibility to radiotherapy and excellent local control can be achieved with advances in radiotherapy and chemotherapy, the effectiveness of these treatments requires further improvements, especially with distant metastasis rates and high local recurrence rates [4]. In fact, 30% ~ 40% of NPC patients will develop distant metastasis within 4 years, and the prognoses become poor upon metastasis [5].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-506 inhibits tumor growth and metastasis in nasopharyngeal carcinoma through the inactivation of the Wnt/β-catenin signaling pathway by down-regulating LHX2

Liang

Zheng

Wang

et al. 2019

J Exp Clin Cancer Res

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Background Epithelial-mesenchymal transition (EMT)-associated proteins play key roles in cancer progression and metastasis with the involvement of microRNAs (miRNAs). This study aims to assess the role of miR-506 working in tandem with LIM Homeobox 2 (LHX2) in EMT and metastasis through the Wnt/β-catenin signaling pathway in nasopharyngeal carcinoma (NPC). Methods Differentially expressed genes associated with NPC were screened using microarray analyses, from which LHX2 was identified. Next, the potential relationship between miR-506 and LHX2 was analyzed. In order to explore the effect of miR-506 or LHX2 on NPC cell proliferation, migration, invasion and apoptosis, serials of mimics, inhibitors or siRNA against LHX2 were transfected into NPC cells. Then, the expression patterns of LHX2, Wnt1, β-catenin, E-cadherin, Vimentin, TCF4 and Twist were determined to assess the influence of miR-506 or LHX2 on EMT as well as the relationship between the Wnt/β-catenin signaling pathway and TCF4. The tumorigenicity and lymph node metastasis (LNM) in xenograft tumors of nude mice were observed. Results The has-miR-506-3p was identified as the down-regulated gene in NPC based on the microarray data while LHX2 was negatively regulated by miR-506. Over-expression of miR-506 or silencing of LHK2 inhibited NPC cell proliferation, migration, invasion, tumorigenicity and LNM but promoted apoptosis indicated by decreased Wnt1, β-catenin, Vimentin, TCF4 and Twist expressions along with increased E-cadherin expressions. Conclusions miR-506 inhibits tumor growth and metastasis in NPC via inhibition of Wnt/β-catenin signaling by down-regulating LHX2, accompanied by decreased TCF4. Taken together, miR-506 targeted-inhibition LHX2 presents a promising therapeutic strategy for the treatment of NPC. Trial registration ChiCTR1800018889 . Registered 15 October 2018. Electronic supplementary material The online version of this article (10.1186/s13046-019-1023-4) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-506 inhibits tumor growth and metastasis in nasopharyngeal carcinoma through the inactivation of the Wnt/β-catenin signaling pathway by down-regulating LHX2

Liang

Zheng

Wang

et al. 2019

J Exp Clin Cancer Res

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show abstract

“…Epstein-Barr virus infection, tumor suppressors, oncogenes, and environmental factors are related to the occurrence of NPC, but the molecular mechanism of its pathogenesis remains to be fully clarified [2]. Although the sensitivity to radiotherapy and good local control can be enhanced with the constant development of chemoradiotherapy, the effectiveness of these treatments needs to be further improved; in particular, the distant metastasis and local recurrence rates stay at high levels [3]. It is reported that 30-40% of NPC patients will have distant metastasis within 4 years, followed by worse prognosis [4].…”

Section: Introductionmentioning

confidence: 99%

Effect of miR-25 on Proliferation of Nasopharyngeal Carcinoma Cells through Wnt/β-Catenin Signaling Pathway

Yuan

Chen

2021

BioMed Research International

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Objective. To investigate the biological role and potential mechanism of miR-25 in nasopharyngeal carcinoma. Methods. The expression of miR-25 in nasopharyngeal carcinoma cell lines was detected by qRT-PCR. The effect of inhibition of miR-25 expression on the proliferative activity of nasopharyngeal carcinoma cell line HONE-1 was examined by CCK-8 method. Flow cytometry was used to detect the effect of miR-25 expression inhibition on the apoptosis rate of nasopharyngeal carcinoma cell line HONE-1. The miRNA target gene prediction site TargetScan predicts the target protein action site of miR-124 and verifies whether miR-25 interacts with the target by luciferase activity assay, qPCR, and Western experiments. The miR-25 inhibitor and target egg gene expression plasmids were cotransfected into HONE-1 cells for rescue experiments to investigate whether miR-25 inhibits proliferation of nasopharyngeal carcinoma cells by target genes. At the same time, qRT-PCR was used to detect the mRNA expression levels of Wnt/β-catenin pathway key proteins TCF4, c-Myc, and Cyclin D1 in different transfected cells. Results. miR-25 expression was upregulated in nasopharyngeal carcinoma cell lines. Functional studies showed that inhibition of miR-25 expression significantly inhibited the proliferation of nasopharyngeal carcinoma cell line HONE-1 ( p < 0.05 ). Inhibition of miR-25 expression by flow cytometry significantly promoted apoptosis ( p < 0.05 ). Detection of dual luciferase activity indicated that DKK3 is a direct target site for miR-25. Western blots showed that inhibition of miR-25 significantly upregulated DKK3 mRNA and protein levels. Supplementation with DKK3 significantly attenuated the inhibitory effect of miR-25 on the proliferation of nasopharyngeal carcinoma cell line HONE-1 ( p < 0.05 ). qRT-PCR found that mRNA levels of TCF4, c-Myc, and Cyclin D1 were significantly upregulated in miR-25-transfected cells compared to control transfection. QRT PCR showed that the mRNA and protein levels of Tcf4, c-myc, and Cyclin D1 were significantly upregulated in miR-25 overexpression-transfected cells. Conclusion. Inhibition of miR-25 expression promotes DKK3 gene expression, and inactivation of Wnt/β-catenin signaling pathway inhibits proliferation and promotes apoptosis of nasopharyngeal carcinoma cells.

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“…Although the radiotherapy can control early stage of NPC, tumor recurrence and distant metastasis are the key difficulties of NPC therapy 4, 5, 6, 7. At present, NPC tumorigenesis and progression are thought to be multistep processes involving multiple genetic and epigenetic changes 8, 9, 10, 11.…”

Section: Introductionmentioning

confidence: 99%

ARHGAP42 promotes cell migration and invasion involving PI3K/Akt signaling pathway in nasopharyngeal carcinoma

Lin

Ding

et al. 2018

Cancer Medicine

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Rho GTPase‐activating protein 42 was identified as an inhibitor of RhoA to maintain normal blood pressure homeostasis. However, the effect of ARHGAP42 in promoting cell malignancy in nasopharyngeal carcinoma is demonstrated in this study. Microarray and real‐time quantitative PCR were used for a mRNA profiling of ARHGAP42 in nasopharyngeal primary and metastatic carcinoma tissues. Western blot and immunohistochemical staining were used for detecting the expression of ARHGAP42 protein in nasopharyngeal carcinoma tissues and cell lines. The overexpression and silence experiments of ARHGAP42 were performed in NPC cell lines using siRNA and expressive plasmid for evaluating cancer cell migration and invasion in vitro. Real‐time quantitative PCR, western blot, and transwell test were employed for with the function of ARHGAP42 and its antisense lncRNA uc010rul. We confirmed the elevated expression of ARHGAP42 in metastatic NPC tissues of mRNA and protein for the first time. Immunohistochemical analysis indicated that NPC patients with highly ARHGAP42 expression were significantly associated with shorter metastasis‐free survival. Knockdown of ARHGAP42 resulted in significant inhibition of nasopharyngeal cancer cell migration and invasion in vitro, and the overexpression of ARHGAP42 showed the opposite effects. In addition, the silence of uc010rul resulted in ARHGAP42 expression decrease and significant inhibition of nasopharyngeal cancer cell migration and invasion. High expression of ARHGAP42 is associated with poor metastasis‐free survival of nasopharyngeal carcinoma patients. ARHGAP42 promotes migration and invasion of nasopharyngeal carcinoma cells in vitro; the antisense lncRNA may be involved in this effect.

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Update zur kombinierten Radio-, Radiochemo- und alleinigen Chemotherapie bei der multimodalen Therapie des Nasopharynxkarzinoms – eine MAC-NPC-Metaanalyse

Cited by 7 publications

References 11 publications

RETRACTED ARTICLE: MicroRNA-506 inhibits tumor growth and metastasis in nasopharyngeal carcinoma through the inactivation of the Wnt/β-catenin signaling pathway by down-regulating LHX2

RETRACTED ARTICLE: MicroRNA-506 inhibits tumor growth and metastasis in nasopharyngeal carcinoma through the inactivation of the Wnt/β-catenin signaling pathway by down-regulating LHX2

Effect of miR-25 on Proliferation of Nasopharyngeal Carcinoma Cells through Wnt/β-Catenin Signaling Pathway

ARHGAP42 promotes cell migration and invasion involving PI3K/Akt signaling pathway in nasopharyngeal carcinoma

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