Objectives MiR‐34 is a tumour suppressor in breast cancer. Neurokinin‐1 receptor (NK1R), which is the predicted target of the miR‐34 family, is overexpressed in many cancers. This study investigated the correlation and clinical significance of miR‐34 and NK1R in breast cancer. Materials and Methods Western blotting, quantitative reverse transcription‐PCR (qRT‐PCR) and luciferase assays were conducted to analyse the regulation of NK1R by miR‐34 in MDA‐MB‐231, MCF‐7, T47D, SK‐BR‐3 and HEK‐293 T cells. MiR‐34b/c‐5p, full‐length NK1R (NK1R‐FL) and truncated NK1R (NK1R‐Tr) expression in fifty patients were quantified by qRT‐PCR and correlated with their clinicopathological parameters. CCK‐8 assays, colony formation assays and flow cytometry were used to measure cell proliferation and apoptosis in MDA‐MB‐231 and MCF‐7 cells transfected with miR‐34b/c‐5p or NK1R‐siRNA and before treatment with or without Substance P (SP), an endogenous peptide agonists of NK1R. The effect of NK1R antagonist aprepitant was also investigated. In vivo xenograft models were used to further verify the regulation of NK1R by miR‐34b/c‐5p. Results Expression levels of miR‐34b/c‐5p and NK1R‐Tr, but not NK1R‐FL, were associated with enhanced malignant potential, such as tumour stage and Ki67 expression. The overexpression of miR‐34b/c‐5p or NK1R silencing potently suppressed cell proliferation and induced G2/M phase arrest and the apoptosis of MDA‐MB‐231 and MCF‐7 cells. The NK1R antagonist aprepitant had similar effects. In vivo studies confirmed that miR‐34b/c‐5p overexpression or NK1R silencing reduced the tumorigenicity of breast cancer. In addition, SP rescued the effects of miR‐34b/c‐5p overexpression or NK1R silencing on cell proliferation and apoptosis in vitro and in vivo assays. Conclusions MiR‐34b/c‐5p and NK1R contribute to breast cancer cell proliferation and apoptosis and are potential targets for breast cancer therapeutics.

Two-dimensional (2D) atomic crystal superlattices integrate diverse 2D layered materials enabling adjustable electronic and optical properties. However, tunability of the interlayer gap and interactions remain challenging. Here we report a solution based on soft oxygen plasma intercalation. 2D atomic crystal molecular superlattices (ACMSs) are produced by intercalating O2+ ions into the interlayer space using the plasma electric field. Stable molecular oxygen layer is formed by van der Waals interactions with adjacent transition metal dichalcogenide (TMD) monolayers. The resulting interlayer gap expansion can effectively isolate TMD monolayers and impart exotic properties to homo-(MoS2[O2]x) and hetero-(MoS2[O2]x/WS2[O2]x) stacked ACMSs beyond typical capacities of monolayer TMDs, such as 100 times stronger photoluminescence and 100 times higher photocurrent. Our potentially universal approach to tune interlayer stacking and interactions in 2D ACMSs may lead to exotic superlattice properties intrinsic to monolayer materials such as direct bandgap pursued for future optoelectronics.

Pancreatic ductal adenocarcinoma (PDAC) is a highly malignant tumor with few biomarkers to guide treatment options. Carbohydrate antigen 19.9 (CA19.9), the most frequently used biomarker for PDAC, is not sensitive and specific enough for the detection of the disease. This study aimed to evaluate serum periostin (POSTN) and CA242 as potential diagnostic biomarkers complementing CA19.9 in detecting pancreatic cancer. Blood samples were from 362 participants, including 213 patients with different stages of PDAC, 75 patients with benign pancreatic disease, and 74 healthy individuals. All samples were randomly divided into a training set and a validation set. Carbohydrate antigen 19.9, CA242, POSTN, as well as carcinoembryonic antigen, were measured by ELISA or automated immunoassay. The receiver operating characteristic curve analysis revealed that the performance of CA19.9 in the validation group were improved by the marker panel composed of CA19.9, POSTN, and CA242, to discriminate early stage PDAC not only from healthy controls (area under the curve [AUC]CA19.9 = 0.94 vs AUCCA19.9 + POSTN + CA242 = 0.98, P < .05) but also from benign conditions (AUCCA19.9 = 0.87 vs AUCCA19.9 + POSTN + CA242 = 0.90, P < .05). In addition, POSTN retained significant diagnostic capabilities to distinguish PDAC CA19.9‐negative from healthy controls (AUCPOSTN = 0.87) as well as from benign conditions (AUCPOSTN = 0.84) in the whole set. This study suggested that POSTN and CA242 are potential diagnostic serum biomarkers complementing CA19.9 in detecting early pancreatic cancer.

Substance P plays a pivotal role in human cancer development and progression by binding to its receptor, neurokinin-1. Neurokinin-1 has 2 isoforms: full-length neurokinin-1 and truncated neurokinin-1, the latter lacking the cytoplasmic terminal 96-amino acid residues of the full-length protein. We have identified 3 candidate miR-206 target sites within the 3′-untranslated region of the full-length neurokinin-1 gene from bioinformatics database searches. In the present study, real-time quantitative polymerase chain reaction was performed to quantify the expression of miR-206, and the expression of neurokinin-1 and full-length neurokinin-1 was detected by immunohistochemistry in 82 clinical cases of breast cancer and paired adjacent normal tissues. The miR-206 target gene was demonstrated by using a dual-luciferase reporter assay, quantitative real-time polymerase chain reaction, and Western blotting. Transwell migration and invasion, colony formation, and proliferation assays were performed to evaluate the effects of miR-206 expression on various aspects of breast cancer cell behavior in vitro. We showed that miR-206 expression is upregulated in breast cancer cell lines and breast cancer tissues when compared to that in adjacent normal tissues, and full-length neurokinin-1 expression inversely correlates with Tumor Lymph Node Metastasis (TNM) stage and lymph node metastasis. Western blotting, quantitative real-time polymerase chain reaction, and dual-luciferase reporter assays demonstrated that miR-206 binds the 3′-untranslated region of full-length neurokinin-1 messenger RNA, regulating protein expression. We showed that the overexpression of miR-206 promotes breast cancer cell invasion, migration, proliferation, and colony formation in vitro. The present study furthers the current understanding of the mechanisms underlying breast cancer pathogenesis and may be useful for the development of novel targeted therapies.