THAP9-AS1 promotes nasopharyngeal carcinoma progression through targeted regulation of the miR-185-5p/SOX13 axis.

Background: It has been reported that long non-coding RNA THAP9-AS1 exerts carcinogenic role by mediating miRNAs and target genes in various human cancers. However, whether THAP9-AS1 influences the progression of nasopharyngeal carcinoma (NPC) remains unknown. Methods: The transcriptional levels of THAP9-AS1 and miR-185-5p were estimated via quantitative real time polymerase chain reaction (qRT-PCR) assay. The protein level of SOX13 was detected with western blotting assay. Additionally, methyl thiazolyl tetrazolium (MTT) assay as well as colony formation assay were utilized to measure cell growth. The apoptotic cells were observed by employing Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) staining analysis, and transwell assay was introduced to test cell migration in addition to invasion. Moreover, the relationship between miR-185-5p and THAP9-AS1 or SOX13 was estimated through dual-luciferase reporter gene assay. Results: THAP9-AS1 was overexpressed in head and neck squamous cell carcinoma (HNSCC) tissues and NPC cells. Besides, silencing of THAP9-AS1 depressed the life processes of NPC cells including cell growth, migration as well as invasion but facilitated cell apoptosis. Further investigation proved that miR-185-5p was the direct target of THAP9-AS1. Besides, the knockdown of THAP9-AS1 notably reduced the transcriptional level of miR-185-5p. Furthermore, THAP9-AS1 served as a sponge of miR-185-5p to modulate the expression of SOX13, which regulated the development of NPC cells. Conclusion: This work verified that THAP9-AS1 promoted NPC cell progression at least partly by mediating the miR-185-5p/SOX13 axis.

Identification of Critical miRNAs as Novel Diagnostic Markers for Laryngeal Squamous Cell Carcinoma.

The prognosis of laryngeal squamous cell carcinoma (LSCC) patients remains poor, and early diagnosis can distinctly improve the long-term survival of LSCC patients. MicroRNAs (miRs) are a group of endogenous, noncoding, 18-24 nucleotide length single-strand RNAs and have been demonstrated to regulate the expression of many genes, thus modulating various cellular biological processes. In this study, we aimed to identify critical diagnostic miRNAs based on two machine learning algorithms. The GSE133632 dataset was acquired from the Gene Expression Omnibus (GEO) datasets, comprising LSCC tissular samples (57 specimens) and matched neighboring healthy mucosa tissular samples (57 specimens). Differentially expressed miRNAs (DEMs) were screened between 57 LSCC specimens and 57 normal specimens. The LASSO regression model and SVM-RFE analysis were carried out for the identification of critical miRNAs. ROC assays were applied to evaluate discriminatory ability. We identified 32 DEMs between LSCC specimens and normal specimens. Two machine learning algorithms confirmed that hsa-miR-615-3p, hsa-miR-4652-5p, hsa-miR-450a-5p, hsa-miR-196a-5p, hsa-miR-21-3p, hsa-miR-139-5p, and hsa-miR-424-5p were critical diagnostic factors. According to the ROC assays, seven miRNAs had an AUC value of >0.85 for LSCC. Taken together, our findings identified seven critical miRNAs in LSCC patients which can be used to diagnose LSCC patients with high sensitivity and specificity. These results must be verified by large-scale prospective studies.

Effects of CD133 expression on chemotherapy and drug sensitivity of adenoid cystic carcinoma.

The cellular resistance of tumors is a major obstacle for successful tumor therapy. Cluster of differentiation (CD)133 plays an important role in the regulation of drug resistance in gastric and colon cancers. However, its effect on chemotherapeutic sensitivity in adenoid cystic carcinoma (ACC) has not been fully explored. The present study discussed the specific role of CD133 in ACC drug­resistant sensitive cells. KOA­1 cells were treated with 5­fluorouracil (5­FU) and pingyangmycin (PYM) to form drug­resistant cell lines. A Cell Counting Kit­8 assay was used to detect the cell survival rate. Cell invasion was measured using a Transwell assay. The expression levels of CD133 were detected by reverse transcription­quantitative (RT­q) PCR. The expression levels of drug­resistant mRNAs and proteins were detected by RT­qPCR and immunofluorescence analyses, respectively. The CD133 were inhibited by small interfering RNA technology. The survival rate and invasive ability of KOA­1 cells were increased following the induction of drug resistance. The expression levels of CD133, multidrug resistance protein (MDR)1 and multidrug resistance­associated protein (MRP)1 were significantly increased in drug­resistant cell lines. Knockdown of CD133 expression in the resistant cell lines, KOA­1/5­FU and KOA­1/PYM, decreased the survival rate and invasive ability. The expression levels of MDR1 and MRP1 were also significantly decreased. Knockdown of CD133 expression in ACC drug­resistant cells could inhibit the viability and invasion of tumors and enhance the sensitivity of drug­resistant cells to chemotherapeutic drugs.

The association of hepatitis C virus infection and thyroid disease: A systematic review and meta-analysis.

Previous studies have reported that hepatitis C virus (HCV) infection may increase the risk of thyroid disease (TD) even thyroid cancer (TC), but quantitative assessments of risk were rare and the results were not consistent. The purpose of this study was to evaluate the impact of HCV infection on TD and TC, and provide clues to explore the relationship between HCV infection and TD and TC. The literature retrieval was performed up to August 20th, 2021 in the database of PubMed, Cochrane library, Web of Science, China National Knowledge Infrastructure and Wang Fang. The risk of HCV for TD or TC was expressed with odds ratio (OR) and 95% confidence intervals (CI). Subgroup analysis was used to explore the source of heterogeneity. Six articles (three studies published as article and three studies published as abstract) were included in this meta-analysis, with a total of 5398 controls and 1925 cases of hepatitis C. The results of meta-analysis found that HCV infection were significantly associated with an increased risk of TD (sum OR = 1.80, 95% CI = 1.54-2.10, P < 0.001, I2 = 74.3%) and TC (sum OR = 16.36, 95% CI = 4.65-57.62, P < 0.001, I2 = 0%). HCV infection may increase the risk of TD and TC. More work is needed in the future to establish a causal role, however an awareness of the possibility of increased risk of TD and TC may lead to earlier diagnosis and better outcomes in patients with hepatitis C.