| Autophagy, also called type II programmed cell death, is a basic biologicalphenomenon that widely spread in eukaryotic cells, the occurrence of autophagy ischaracterized by the appearance of the autophagosome that wrapped long life ofproteins and organelles by cytoplasmic membrane structure, is a series of biochemicalprocesses of the degradation of cellular macromolecules and organelles depend onlysosomal. Since addicted as "scavenger" of cells, autophagy can maintain thebalance of protein metabolism and the stability of intracellular environment[1];Autophagy can naturally remove cellular waste, update cell structure. Molecularstudies indicated that the incidence, development and apoptosis of cancer were relatedto the inhibition of the cell apoptosis and the unlimited proliferation of the cell.Autophagy as type II programmed cell death, was closely related to apoptosis, theabnormal regulation of autophagy was closely related to the occurrence anddevelopment of the tumor. Currently, a variety of malignant tumors have been foundto the change of autophagy activity[2]. Autophagy was the process of regulated by avariety of factors. The abnormal regulation of certain genes can cause the change ofautophagic activity. Beclin1was autophagy-related genes that interaction with Bcl-2,it can start the process of autophagy, but MAP1LC3protein as a marker of autophagy,with autophagy specificity. The two genes involved in the regulation of autophagy activity as autophagy-related genes, and played important roles in tumor occurrenceand development. By studying the mechanism of autophagy in the development of thetumor would provide a new strategy for cancer therapy. Squamous cell carcinoma ofthe external auditory canal and the auricle was one of the most common malignanciesin the ear, about autophagy and the autophagy gene Beclin1, MAP1LC3expression insquamous cell carcinoma of the external auditory canal and the auricle and theclinical significance was currently still blank.ObjectiveDetected the expression of autophagy-related gene Beclin1and MAP1LC3insquamous cell carcinoma of the external auditory canal and the auricle, in the externalauditory canal papilloma and the normal ear skin tissue. And discuss the relationshipbetween the expression of the two factors and relationship between the two factorswith the clinical pathological features of squamous cell carcinoma of the externalauditory canal and the auricle. Explore the role of Beclin1and MAP1LC3played insquamous cell carcinoma of the external auditory canal and the auricle, as achievedproviding a theoretical basis for targeted therapy of squamous cell carcinoma byinducing cell occurred initiative death. And further analysis the relationship betweenthe expression of the two factors in squamous cell carcinoma of the external auditorycanal and the auricle.MethodsMaterials were divided into three groups, immunohistochemistry was used todetect the expression of Beclin1and MAP1LC3in42cases of squamous cellcarcinoma of the external auditory canal and the auricle,38cases of external auditorycanal papilloma,40exceptions to the normal ear skin tissue. Statistical dates wereanalyzed by SPSS17.0-statistical software. The strength of the two factors expressionin squamous cell carcinoma, papilloma, and normal tissue of these three tissues arerepresented by mean±standard deviation (x±s), then using the one-way ANOVA.The two factors expression in different diseased parts, T stage, clinical stage and lymph node metastasis of the squamous cell carcinoma are used2test, thecorrelation between the two indexes using Spearman rank correlation test. P<0.05was considered statistically significant.Results1. The integrated optical density（IOD）values of Beclin1in Squamous cellcarcinoma of the external auditory canal and the auricle, the external auditory canalpapilloma and the normal ear skin tissue were65.824±4.999,121.167±13.169,125.145±22.025. The difference was significantly (P=0.000).The IOD values ofMAP1LC3in squamous cell carcinoma of the external auditory canal and the auricle,the external auditory canal papilloma and the normal ear skin tissue were68.954±3.443,123.671±6.808,125.794±13.005. The difference was significantly(P=0.000). The expression of Beclin1、MAP1LC3in squamous cell carcinoma wassignificantly lower than the expression in papilloma group and normal ear skin group,The difference was significantly (P<0.05). There was no difference between theexpression of Beclin1and MAP1LC3in the external auditory canal papilloma and thenormal ear skin tissue, the difference was not statistically significant (P>0.05).2. The expression rates of Beclinl in squamous cell carcinoma of the externalauditory canal and the auricle and were set at25.00%,22.22%, the difference was notstatistically significant (P>0.05). The expression rates of MAP1LC3in squamouscell carcinoma of the external auditory canal and the auricle were set at29.17％,16.67%.The difference was not statistically significant (P>0.05).3. The expression rates of Beclinl in squamous cell carcinoma of the externalauditory canal and the auricle in stage1-2and stage3-4were25.71%,28.57%, thedifference was not statistically significant (P>0.05). The expression rates ofMAP1LC3in squamous cell carcinoma of the external auditory canal and the auriclein stage1-2and stage3-4were in T1-2, T3-4were22.86%,14.29%, the differencewas not statistically significant (P>0.05).4. The expression rates of Beclinl in squamous cell carcinoma of the externalauditory canal and the auricle with lymph node metastasis group, without lymph node metastasis group the rates were11.11%,41.67%, the difference between the twogroups was significantly (P<0.05). The expression rates of MAP1LC3in squamouscell carcinoma of the external auditory canal and the auricle with lymph nodemetastasis group, without lymph node metastasis group the rates were5.56%,37.50%,the difference between the two groups was significantly (P<0.05).5. The expression rates of Beclinl in squamous cell carcinoma of the externalauditory canal and the auricle in the early and late stage were30.43%,15.79%, thedifference was not statistically significant (P>0.05).The expression rates ofMAP1LC3in squamous cell carcinoma of the external auditory canal and the auriclein the early and late stage were17.39%,21.05%, the difference was not statisticallysignificant (P>0.05).6. The expression of Beclinl and MAPlLC3in squamous cell carcinoma of theexternal auditory canal and the auricle were no correlation (P>0.05).Conclusions1. The expression rates of Beclin1, MAP1LC3in squamous cell carcinoma ofthe external auditory canal and the auricle were low. And the expression rates wereparticularly lower in squamous cell carcinoma with lymph node metastasis group.Autophagy played a role of inhibition in the occurrence and development ofsquamous cell carcinoma of the external auditory canal and the auricle and theprocess of lymph node metastasis addicted in tumor.2. The expression of Beclin1, MAP1LC3in squamous cell carcinoma of theexternal auditory canal and the auricle were not significantly associated with differenttumor disease site, T grading and clinical stage, but significantly associated withlymph node metastasis. The detection of the two markers could help addicting theefficacy, prognosis and recurrence monitoring of squamous cell carcinoma of theexternal auditory canal and the auricle.3. There was no significant correlation between the expression of Beclin1,MAP1LC3in squamous cell carcinoma of the external auditory canal and the auricle.4. Through autophagy inducing the squamous cell carcinoma cell to initiative died could be a new strategy for targeted therapy of squamous cell carcinoma of theexternal auditory canal and the auricle. |
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