ABSTRACT
Tongue cancer remains a massive threat to public health due to the high rate of metastasis. Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor ß1 (TGFß1), has been regarded as a significant contributor to cancer invasion and migration. In our previous study, long noncoding RNA (lncRNA) MALAT1/miR-124/JAG1 axis modulates the growth of tongue cancer. In addition to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), another lncRNA, urothelial cancer associated 1 (UCA1), can promote EMT and cancer metastasis. In the present study, UCA1 was overexpressed in tongue cancer tissues and cell lines. UCA1 overexpression was correlated to the poorer prognosis of patients with tongue cancer. UCA1 knockdown significantly suppressed TGFß1-induced tongue cancer cell invasion and EMT by decreasing vimentin and increasing E-cadherin. Regarding the molecular mechanism, UCA1 could directly bind to microRNA-124 (miR-124) and negatively regulate each other. UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFß1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling. Moreover, miR-124 inhibition partially impaired the effect of UCA1 knockdown. In tongue cancer tissues, miR-124 expression was remarkably decreased, whereas JAG1 mRNA expression was increased. miR-124 was negatively correlated with UCA1 and JAG1. UCA1 and JAG1 were positively correlated. In summary, we provided a novel mechanism by which the EMT process and cancer cell invasion in tongue cancer could be modulated from the perspective of lncRNA-miRNA-mRNA regulation.
Subject(s)
Epithelial-Mesenchymal Transition/genetics , MicroRNAs/genetics , RNA, Long Noncoding/genetics , Tongue Neoplasms/genetics , Cell Line, Tumor , Epithelial-Mesenchymal Transition/drug effects , Female , Gene Expression Regulation, Neoplastic , Humans , Jagged-1 Protein/metabolism , Kaplan-Meier Estimate , Lymphatic Metastasis/genetics , Male , MicroRNAs/metabolism , Middle Aged , RNA, Long Noncoding/metabolism , Receptors, Notch/genetics , Receptors, Notch/metabolism , Tongue Neoplasms/mortality , Tongue Neoplasms/pathology , Transforming Growth Factor beta1/metabolism , Transforming Growth Factor beta1/pharmacologyABSTRACT
Objective @#To summarize experience treating dog bites in the oral and maxillofacial regions of children and provide a reference for clinical practice.@*Methods @#Nineteen children with dog bite wounds in the maxillofacial region were treated from July 2011 to June 2018 with primary debridement and suturing. A rabies vaccine, tetanus vaccine and human immunoglobulin as a passive immune agent were given via intramuscular injection. Anti-inflammatory therapy with amoxicillin and clavulanate potassium or other antibiotics. Follow-up observation and a retrospective analysis of the treatment effect were carried out.@*Results@#After treatment, among the 19 pediatric patients, 18 cases showed primary healing and 1 case showed secondary healing. The follow-up period ranged from six months to seven and a half years. No cases of rabies occurred.@*Conclusion @#For the treatment of patients with maxillofacial dog bite wounds, the first stage debridement and suture can reduce the scar after operation and is beneficial to the recovery of face.
ABSTRACT
We wish to retract our research article entitled "Long noncoding RNA MALAT1 interacts with miR124 and modulates tongue cancer growth by targeting JAG1" published in Oncology Reports 37 20872094, 2017. Following the publication of this article, it was drawn to our attention that this paper bore numerous similarites with an article published previously in the journal OncoTargets and Therapy. Although all the data reported in our study were original, we recognize that it was not appropriate that we should have modelled our paper on previously published articles as a template on which to base the writing of our paper. Therefore, we have agreed to follow the Editor's recommendation that this paper be retracted from the publication. All the named authors agree to this retraction. We sincerely apologize to the Editor and the readership of the Journal for our action, and regret any inconvenience this has caused. [the original article was published in the Oncology Reports 37: 20872094, 2017; DOI: 10.3892/or.2017.5445].
ABSTRACT
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), was the earliest discovered to be correlated with cancer and contributes to the initiation and development of several types of tumors. Dysregulation of MALAT1 expression is frequently observed in many types of cancer such as gastric cancer, esophageal squamous cell carcinoma and glioma. To date, the role of MALAT1 and the underlying mechanisms in tongue cancer development remain unclear. In the present study, we studied the influence of MALAT1 on tongue cancer cell lines and clinical tongue cancer samples so as to detect its function and the underlying mechanism. In the present study, lncRNA-MALAT1 was specifically upregulated in tongue cancer cell lines and overexpression promoted tongue cancer cell growth by targeting miR-124. Knockdown of MALAT1 suppressed the growth and invasion of human tongue cancer cells and inhibited metastasis in vitro and in vivo. In addition, miR-124-dependent jagged1 (JAG1) regulation was required for MALAT1-induced tongue cancer cell growth. Our data revealed that MALAT1 inhibited tongue cancer cell growth and metastasis through miR-124-dependent JAG1 regulation. In conclusion, we revealed that MALAT1 may play an oncogenic role by increasing proliferation and metastasis of tongue cancer and is a potential therapeutic target in human tongue cancer.
Subject(s)
Jagged-1 Protein/biosynthesis , MicroRNAs/biosynthesis , RNA, Long Noncoding/genetics , Tongue Neoplasms/genetics , Apoptosis/genetics , Cell Line, Tumor , Cell Proliferation/genetics , Female , Gene Expression Regulation, Neoplastic , Humans , Jagged-1 Protein/genetics , Male , MicroRNAs/genetics , RNA, Long Noncoding/metabolism , Tongue Neoplasms/pathologyABSTRACT
BACKGROUND: TGFß1 and Smad3 play an important role in the process of EMT. TGFß1 regulates the expression of Jagged1 by modulating Notch signaling. Jagged1 is related to tumor invasion, metastasis, chemotherapy resistance, and tumor immune escape. The aims of this study are to examine deregulation of TGFß1-Smad3-Jagged1-Notch1-Slug signaling in TSCC and to investigate its roles in TSCC progression. MATERIALS AND METHODS: Notch1, Smad3, Jagged1 and Slug proteins and mRNA expression were detected in specimens from 89 cases of patients. We analyzed the correlation between their expressions and histological grade, clinical stage and lymph node metastasis. RESULTS: Notch1, Smad3, Jagged1 and Slug mRNA expressions in TSCC were higher than normal tissue (P <0.05). The protein expression of Notch1 and Smad3 in TSCC were higher (χ(2) =7.30, P <0.01 and χ(2) = 5.84, P <0.05). Notch1 and Smad3 expressions were correlated with clinical stage (χ(2) =18.81, P<0.01; χ(2) =22.29, P<0.01), but not Jagged1 (χ(2) =0.53, P>0.05). The Slug protein expression was correlated with clinical stage. The positive rate of Notch1 was higher in lymph node metastases positive cases (χ(2) =7.30, P<0.01). Moreover, higher expression of Jagged1 was found in lymph node positive cases (χ(2) =10.82, P<0.01). CONCLUSIONS: The key protein expression in TGFß1-Smad3-Jagged1-Notch1-Slug signaling pathway significantly correlated with the clinicopathological features of TSCC patients. It's potential as a biomarker and a novel therapeutic target for TSCC patients at risk of metastasis. It may play an irreplaceable role in TSCC progression which may attribute to promoting EMT which enhances cell migration, invasion and metastasis.
