The role of interferon-stimulated gene 15 in the occurence and progression of cervical squamous cell carcinoma.

To identify molecular markers for early diagnosis and new targets for treatment of cervical squamous cell carcinoma. Our study involved 52 carcinoma tissues that were confirmed pathologically as cervical squamous cell carcinoma (CSCC) at the Fourth Hospital of Hebei Medical University in 2021. We obtained 36 control specimens from patients who had undergone hysterectomy for benign uterine diseases in 2021, with no cervical lesions as confirmed by pathology. Total RNA was extracted from all the samples. Reverse transcription and quantitative real-time PCR were performed. Immunohistochemical staining for interferon-stimulated gene 15 (ISG15) protein was performed. Descriptive analyses including mean and standard deviation were used to compare different groups. For data that do not conform to normal distribution, we use Wilcox rank sum test to make statistics to compare different groups with the median and interquartile. Mann Whitney U test was used to compare non-parametric continuous data, and categorical variables were analyzed using chi-square test. Receiver operating characteristic (ROC) curve was used to evaluate the possibility of using ISG15 as a new biomarker for cervical squamous cell carcinoma. Compared with normal cervical tissues, mRNA expression of ISG15 in cervical cancer tissues was significantly lower (P<0.01); mRNA expression was significantly lower in patients with nerve invasion (P<0.05). Difference in ISG15 protein expression was statistically significant (no expression/low expression) in the cancer samples compared to normal tissues (P<0.01). The area under ROC curve was 0.810 (P<0.001) and the sensitivity and specificity were 75% and 54%, respectively. Spearman's correlation analysis showed that ISG15 mRNA was positively correlated with protein expression (r=0.358, P=0.001). Deficiency of ISG15 may be associated with the occurrence and progression of CSCC. It could be used as a potential tumor marker in research and treatment of CSCC.

LncRNA MEG3 inhibits proliferation and promotes apoptosis of osteosarcoma cells through regulating Notch signaling pathway.

OBJECTIVE: To explore the effect of long non-coding ribonucleic acid (lncRNA)-maternally expressed gene 3 (MEG3) on the Notch signaling pathway, and its influences on the proliferation and apoptosis of osteosarcoma MG-63 cells. MATERIALS AND METHODS: LncRNA MEG3 was overexpressed in osteosarcoma MG-63 cells, and the cells were divided into Blank group, Len-con group, and Len-MEG3 group. The expression level of MEG3 in each group was detected via quantitative Polymerase Chain Reaction (qPCR), the cell proliferation level in each group was detected via Cell Counting Kit-8 (CCK-8) assay, and the apoptosis in each group was detected via Hoechst 33258 staining. Moreover, the content of the inflammatory factors in each group was determined using the Enzyme-Linked Immunosorbent Assay (ELISA), and the expression levels of apoptosis-related proteins and Notch signaling pathway-related proteins were determined through Western blotting. RESULTS: The expression level of lncRNA MEG3 in Len-MEG3 group was significantly higher than that in the Blank group and Len-con group (p<0.01). The overexpression of lncRNA MEG3 could significantly weaken the proliferation (p<0.01) and enhance the apoptosis of osteosarcoma cells (p<0.01). The overexpression of lncRNA MEG3 could significantly increase the content of the inflammatory factor interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) (p<0.01), and remarkably decrease the content of the anti-inflammatory factor IL-10 in osteosarcoma cells (p<0.01). Besides, the overexpression of lncRNA MEG3 could evidently raise the expression of Caspase3 (p<0.01) and reduce the Bcl-2/Bax expression in osteosarcoma cells (p<0.01). Finally, the overexpression of lncRNA MEG3 could remarkably reduce the protein expressions of Jagged1, Notch1, and NICD1 in osteosarcoma cells (p<0.01). CONCLUSIONS: The overexpression of lncRNA MEG3 can inhibit the proliferation and promote the apoptosis of osteosarcoma MG-63 cells by suppressing the Notch signaling pathway.

Expression of FOXP3 in esophageal squamous cell carcinoma relating to the clinical data.

Forkhead box protein 3 (FOXP3) has been studied as a biomarker in many human malignancies recently. But in esophageal squamous cell carcinoma (ESCC) the studies are limited. In this study, expression of FOXP3 in ESCC tissue was evaluated in relation to the clinical data. Detection of FOXP3 mRNA was made by using quantitative real-time PCR while protein expression was assessed by immunocytochemistry (n = 112). The results were correlated to the clinical data including age, gender, carcinoma size, carcinoma differentiation, lymphatic invasion and pathological stage. A significantly higher FOXP3 expression in tumors was confirmed than in normal-appearing mucosa. The FOXP3 mRNA and protein expressions were higher in advanced stages (stage II B and III) than in early stages (stage I and stage II A). A significantly higher FOXP3 expression in tumors with lymph node metastasis was also confirmed than in those without lymph node metastasis. No significant correlation was found in age, gender, carcinoma size, or carcinoma differentiation. These results suggest that expression of FOXP3 was higher in ESCC tissue and was closely correlated to lymphatic invasion and pathological stage. It may imply that FOXP3 might play an important role in esophageal carcinoma progression.