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Objective: To investigate 38 Y-chromosome short tandem repeat (Y-STR) genetic polymorphisms in Beijing Han and analyze the genetic distance with neighboring or linguistically similar populations. Materials and Methods: In the study, we selected 531 unrelated male individuals of Beijing Han, and the results were statistically analyzed by testing with GSTAR™ 41Y reagents. Results: The allele peak heights were balanced among the Y loci, the amplified fragment ranged from 100 to 500 bps. A total of 531 haplotypes were detected in 531 samples. Eight null genotypes were observed on locus DYS448. One and three double alleles were observed on single-copy locus DYS576 and DYS19, respectively. DYS385 a/b, DYF387S1 a/b, and DYS527 a/b were more common in double copies, but 3, 13, and 11 triple alleles were detected, respectively. The gene diversity values of Y-STRs except DYS391, DYS438, and DYS645 were >0.5. Twenty-seven Y-STRs of Beijing Han population were selected for genetic distance comparison with 17 populations including Changchun Han, with Rst values ranging from 0.0002 to 0.1703. Conclusion: The 38 Y-STRs in this study have strong male lineage identification ability and have great potential for individual identification, kinship identification, Y-STR database construction, and genetic relationship research. [ABSTRACT FROM AUTHOR]

The CXC chemokines belong to a family which includes 17 different CXC members. Accumulating evidence suggests that CXC chemokines regulate tumor cell proliferation, invasion, and metastasis in various types of cancers by influencing the tumor microenvironment. The different expression profiles and specific function of each CXC chemokine in head and neck squamous cell carcinoma (HNSCC) are not yet clarified. In our work, we analyzed the altered expression, interaction network, and clinical data of CXC chemokines in patients with HNSCC by using the following: the Oncomine dataset, cBioPortal, Metascape, String analysis, GEPIA, and the Kaplan–Meier plotter. The transcriptional level analysis suggested that the mRNA levels of CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL8, CXCL9, CXCL10, CXCL11, and CXCL13 increased in HNSCC tissue samples when compared to the control tissue samples. The expression levels of CXCL9, CXCL10, CXCL11, CXCL12, and CXCL14 were associated with various tumor stages in HNSCC. Clinical data analysis showed that high transcription levels of CXCL2, CXCL3, and CXCL12, were linked with low relapse-free survival (RFS) in HNSCC patients. On the other hand, high CXCL14 levels predicted high RFS outcomes in HNSCC patients. Meanwhile, increased gene transcription levels of CXCL9, CXCL10, CXCL13, CXCL14, and CXCL17 were associated with a higher overall survival (OS) advantage in HNSCC patients, while high levels of CXCL1, and CXCL8 were associated with poor OS in all HNSCC patients. This study implied that CXCL1, CXCL2, CXCL3, CXCL8, and CXCL12 could be used as prognosis markers to identify low survival rate subgroups of patients with HNSCC as well as be potential suitable therapeutic targets for HNSCC patients. Additionally, CXCL9, CXCL10, CXCL13, CXCL14, and CXCL17 could be used as functional prognosis biomarkers to identify better survival rate subgroups of patients with HNSCC. [ABSTRACT FROM AUTHOR]

Tumor cells switch from an epithelial to a mesenchymal-like phenotype, which represents a key hallmark of human cancer metastasis, including gallbladder cancer (GBC). A large set of microRNAs (miRNAs/miRs) have been studied to elucidate their functions in initiating or inhibiting this phenotypic switching in GBC cells. In this paper, we attempted to identify the expression pattern of the miR-214/−3120 cluster and its mode of action in the context of GBC, with a specific focus being placed on their effects on EMT and autophagy in GBC cells. Human GBC cells GBC-SD were assayed for their migration, invasion, and autophagy using the Transwell chamber system, MDC staining, and transmission electron microscopy. The tumorigenicity and metastatic behavior of GBC-SD cells were tested in nude mice. The expression of EMT- and autophagy-specific markers (E-cadherin, N-cadherin, vimentin, ATG5, LC3II/LC3I, and Beclin1) was analyzed in cultured GBC-SD cells and in human GBC-SD xenografts. The E2F3 luciferase reporter activity in the presence of miR-214/−3120 was evaluated by a dual luciferase assay. The miR-214/−3120 was downregulated in GBC. Exogenous miR-214/−3120 inhibited the phenotypic switching of GBC cells from epithelial to mesenchymal, prevented autophagy, and suppressed the tumorigenicity and metastatic behavior of GBC-SD cells in vitro and in vivo. E2F3 was demonstrated to be the target gene of miR-214/−3120, and its knockdown in part mimicked the effect of miR-214/−3120 on the EMT, autophagy, tumorigenicity, and metastatic behavior of GBC-SD cells. These results demonstrated that the miR-214/−3120 cluster blocks the process of EMT and autophagy to limit GBC metastasis by repressing E2F3 expression. • miR-214 and miR-3120 compose a miRNA cluster and are both downregulated in gallbladder cancer (GBC). • The miR-214/−3120 cluster inhibits the expression of E2F3 in GBC cells. • The miR-214/−3120 cluster prevents tumor cell switch from an epithelial to a mesenchymal-like phenotype and autophagy repressing SEMA6B expression in GBC. • Restoring miR-214/−3120 microRNA cluster may provide a means of targeting mesenchymal-like, invasive tumor cells in GBC. [ABSTRACT FROM AUTHOR]