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Background: Vasculogenic mimicry (VM) refers to the direct formation of microcirculatory ducts by invasive malignant tumors via cellular phenotypic transformation. However, there is a lack of VM‐based biomarkers for breast cancer. Methods: We obtained transcriptomic expression data, single cell sequencing data, and clinical data of patients from The Cancer Genome Atlas Program (TCGA) database and GEO database, performed single cell analysis to obtain specific type annotations of breast cancer cells and analyzed their spatial expression analysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) and gene ontology (GO) analyses as well as Gene Set Enrichment Analysis (GSEA) analyses were performed to clarify the biological pathways and tumor functional enrichment relationships of the major expressed genes of VM in the breast cancer bulk data specimens. VM biomarkers were constructed. Meanwhile, the relationship between VM scores and tumor immune infiltration in breast cancer was analyzed using MCPcounter and ssGSEA methods. In addition, we assessed the specific relationship between NDRG1, a key VM gene in breast cancer, and tumor colonization, adhesion and invasion by biological experiments in breast cancer cell lines. Results: The main cell types of breast cancer (BRCA) samples were annotated by single cell transcriptome analysis. Most of the VM‐high group was present in epithelial cells, whereas the VM‐low group was present in immune and stromal cells. Multiple tumor pathways such as TGFβ p53 and MAPK were closely associated with VM‐mediated breast cancer infiltration and invasion. A prognostic model of breast cancer based on VM key genes was constituted. Prognostic stratification of breast cancer was successfully achieved for the TCGA‐BRCA and GSE58812 datasets. Through immune infiltration analysis, we found that differential expression of VM markers was associated with multiple immune cell regulation. In MDA‐MB‐231 and MDA‐MB‐453 cell lines, we found that the NDRG1 gene significantly promoted colony formation of breast cancer cells. Conclusion: Our constructed VM‐related gene‐based model of breast cancer biology holds promise for prognostic prediction and patient stratification of breast cancer. This may provide a potentially clinically valuable aid in promoting a deeper understanding of the biological regulation of VM in breast cancer and exploring the specific mechanisms of tumor angiogenesis and breast cancer development. [ABSTRACT FROM AUTHOR]

Paclitaxel (PTX) resistance is a key cause of chemotherapy failure in patients with triple negative breast cancer (TNBC). The aim of this study is to investigate the effect and mechanism of long non‐coding RNA (lncRNA) on the PTX resistance of TNBC cells through autophagy. MDA‐MB‐231 cells are used to induce the PTX‐resistant TNBC cell line MDA‐MB‐231.PR (MDR) by increasing dose intermittently. Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to validate the mRNA levels of phosphoinositide‐3‐kinase class 3 (PIK3C3), miR‐361‐5p and lncRNA PRKCQ‐AS1 in the cells, and Western blot analysis was used to detect the protein expressions of PIK3C3, autophagy‐related, drug‐resistant and apoptosis‐related genes. MDC staining detected the formation of autophagic vacuoles. The interactions between miR‐361‐5p and PIK3C3 and between lncRNA PRKCQ‐AS1 and miR‐361‐5p were verified by dual‐luciferase assay. Cell viability, apoptosis, migration and invasion were assessed by performing MTT, flow cytometry assay, and transwell assay. The mRNA level of miR‐361‐5p and the autophagy and drug resistance levels of TNBC PTX‐resistant cells were significantly up‐regulated. miR‐361‐5p could target autophagy‐related gene PIK3C3, and overexpression of miR‐361‐5p could down‐regulate PIK3C3 protein expression and autophagy level and PTX resistance of MDR cells. LncRNA PRKCQ‐AS1 was selected through bioanalysis, and miR‐361‐5p could target lncRNA PRKCQ‐AS1. In addition, lncRNA PRKCQ‐AS1 level was up‐regulated in TNBC PTX‐resistant cells, and knockdown of lncRNA PRKCQ‐AS1 could weaken autophagy and drug resistance level and could promote cell apoptosis. Overexpression of lncRNA PRKCQ‐AS1 reversed the pro‐apoptotic effect and down‐regulation of autophagy and resistance levels was induced by miR‐361‐5p. In vivo experiments were performed to verify the role of lncRNA PRKCQ‐AS1. We demonstrate that down‐regulation of lncRNA PRKCQ‐AS1 weakened PTX resistance and promoted cell apoptosis by miR‐361‐5p/PIK3C3 mediated autophagy. [ABSTRACT FROM AUTHOR]

Objectives We aimed to determine the predictive factors for central compartment lymph node metastasis ( LNM) in papillary thyroid microcarcinoma ( PTMC). Design and patients We undertook a retrospective study of 291 patients treated for PTMC. The following criteria were assessed to predict the presence of central compartment LNM: sex, age, tumour multifocality, tumour size, tumour bilaterality, extracapsular spread ( ECS), lateral neck LNM, coexistence of chronic lymphocytic thyroiditis, BRAFV600E mutation and ultrasonography ( US) features. Univariate and multivariate analyses were performed to identify clinicopathological characteristics and US findings in predicting central compartment LNM from PTMC. Results The central compartment LNM affected 133 (45·7%) of 291 patients. With use of univariate and multivariate analyses, male gender ( OR 2·020; P = 0·039), tumour size (>5 mm) ( OR 3·687; P = 0·015), ESC ( OR 2·330; P = 0·044), lateral LNM ( OR 15·075; P = 0·000) and BRAFV600E mutation ( OR 2·464; P = 0·000) were independently correlated with central compartment LNM. Age, tumour multifocality, tumour bilaterality, coexistence of chronic lymphocytic thyroiditis and US characteristics were not significantly related to the presence of central compartment LNM. We have also developed a nomogram to predict the probability of central compartment LNM for an individual patient. The sensitivity was 71·9% and specificity was 70·3%, with an under the receiver operating characteristic ( ROC) curve of 0·772. Conclusions A prophylactic neck dissection of the central compartment should be considered particularly in PTMC patients with male gender, a >5 mm tumour size, ECS of the tumours, lateral LNM and positive BRAFV600E mutation. [ABSTRACT FROM AUTHOR]