Atomic-level modulation of electron density in iron sulfides for enhancing sodium storage kinetics.

Iron sulfides (FeS2) are promising anode materials for sodium ion batteries (SIBs); however, their inferior electronic conductivity, large volume swelling, and sluggish sodium ion diffusion kinetics lead to unsatisfactory rate performance and cycling durability. Heteroatom doping plays a crucial role in modifying the physicochemical properties of FeS2 anodes to enhance its sodium storage. Herein, ultra-fine Ni-doped FeS2 nanocrystals derived from a metal-organic framework (MOF) and in-situ anchored on a nitrogen doped carbon skeleton (Ni-FeS2@NC) are proposed to enhance both structural stability and reaction kinetics. Material characterization, electrochemical performance, and kinetics analysis demonstrate the critical role of Ni doping in sodium storage, particularly in accelerating Na+ diffusion efficiency. The N-doped carbon derived from the MOF can buffer the volume expansion and enhance the structural stability of electrode materials during sodiation/desodiation processes. As expected, Ni-FeS2@NC exhibits a high reversible capacity of 656.6 ± 65.1 mAh g-1 at 1.0 A g-1 after 200 cycles, superior rate performance (308.8 ± 6.0 mAh g-1 at 10.0 A g-1), and long-term cycling durability over 2000 cycles at 1.0 A g-1. Overall, this study presents an effective approach for enhancing the sodium storage performance and kinetics of anode materials for high efficiency SIBs.

Relationship between COVID-19 vaccine hesitancy and willingness to pay for the booster dose of COVID-19 vaccine of oncology patients in Taizhou, China.

OBJECTIVE: This population-based study aimed to determine the hesitancy and willingness to pay (WTP) for the booster dose of a coronavirus disease (COVID-19) vaccine among patients with cancer in Taizhou, China. PATIENTS AND METHODS: A self-administered online questionnaire was administered to patients with cancer in Taizhou, China. The chi-square test, binary logistic regression model were used to evaluate the WTP for the booster dose of a COVID-19 vaccine. The minimum sample size was 218, determined by G*Power software (latest ver. 3.1.9.7). A total of 354 patients received the survey, and 256 (72.3%) patients responded. RESULTS: Overall, 69.9% (179/256) of respondents were willing to pay for the booster dose, and 78.8% (141/179) of these patients were willing to pay 1-99 CNY. Furthermore, 50.4% (129/256) of respondents were hesitant to receive a COVID-19 vaccine. Being unhesitant was significantly associated with WTP for the booster dose (aOR: 3.040; 95% CI: 1.669-5.540). CONCLUSION: Hesitant patients with cancer had a lower WTP for the booster dose against COVID-19 than non-hesitant participants. These results imply that further health education programmes are essential to decrease the hesitancy of patients with cancer and enhance booster dose vaccination rates for public health improvements.KEY MESSAGESOur research showed that 70% of patients with cancer are willing to pay for the booster dose of the COVID-19 vaccine, and most are willing to pay less than 100 CNY, and this result reflects the economic value and affordability of the third dose of vaccination.COVID-19 vaccine-hesitant patients with cancer had a lower willingness to pay for a booster dose against COVID-19 than non-hesitant participants and few patients are still unwilling to pay among patients do not hesitate to receive the third dose.Therefore, promoting willingness to pay among oncology patients and addressing vaccine hesitancy remains key.

MiR-1236-3p serves as a new diagnostic and prognostic biomarker for gastric cancer.

BACKGROUND: The microRNA plays an important role in tumor progression. MiR-1236-3p acts as a tumor suppressor in various malignancies. OBJECTIVE: The aim of present study was to explore the expression of miR-1236-3p in gastric cancer (GC) and its correlation with clinicopathological features, and evaluate the feasibility of using it as a prognostic biomarker in GC. METHODS: Seventy-six pairs of tissue specimens were collected from GC patients. MiR-1236-3p expression level was detected by using qRT-PCR. The diagnostic value of miR-1236-3p was evaluated by receiver operating characteristic curve, and Kaplan-Meier method was used to analyze the overall survival. Prognosis analysis was performed using multivariate cox proportional hazards regression analysis. RESULTS: The expression of miR-1236-3p was significantly reduced in tumor tissues (P< 0.001). In addition, miR-1236-3p expression was correlated with TNM stage (P= 0.001), lymph node metastasis (P= 0.005) and differentiated degree (P= 0.001). The area under the curve was 0.7016, and its specificity and sensitivity were 60.53% and 73.68%. Kaplan-Meier survival curves showed that patients with high miR-1236-3p expression had better overall survival than those with low expression (P= 0.0190). Multivariate Cox regression analysis showed that the miR-1236-3p expression (P= 0.033) was an independent prognostic factor for overall survival of GC prognosis. CONCLUSIONS: The study showed that miR-1236-3p is downregulated in GC tissues, and low expression of miR-1236-3p is associated with a poor prognosis in GC. It may be a new diagnostic and prognostic biomarker for GC.

Correction to: ZEB1­AS1 initiates a miRNA­mediated ceRNA network to facilitate gastric cancer progression.

[This corrects the article DOI: 10.1186/s12935-019-0742-0.].

ZEB1-AS1 initiates a miRNA-mediated ceRNA network to facilitate gastric cancer progression.

BACKGROUND: Currently, cancer-related competing endogenous RNA (ceRNA) networks are attracting significant interest. As long noncoding RNA ZEB1-AS1 has been reported to function as an oncogene due to sponging microRNAs (miRNAs) in several cancers, we hypothesized that it could interact with specific miRNAs to form regulatory networks and facilitate the growth of gastric cancer (GC). METHODS: MiRNAs interacting with ZEB1-AS1 were screened for and selected by bioinformatics analysis. Overexpression or repression of ZEB1-AS1 was performed to determine whether it could regulate selected miRNAs. Quantitative real-time polymerase chain reactions (qPCR) validated the expression profiles of ZEB1-AS1 and miR-149-3p in GC cell lines and tissue. Statistical analysis determined the clinical significance of ZEB1-AS1 in relation to miR-149-3p. Cell counting, wound healing and transwell assays were performed to assess cell proliferation, migration and invasion. A luciferase reporter assay was utilized to confirm the putative miR-149-3p-binding sites in ZEB1-AS1. RESULTS: Briefly, bioinformatics analysis inferred that ZEB1-AS1 interacts with miR-204, miR-610, and miR-149. Gain- or loss-of function assays suggested that ZEB1-AS1 negatively regulates miR-149-3p, miR-204-5p and miR-610 in GC cells. Validated by qPCR, ZEB1-AS1 was up-regulated and miR-149-3p down-regulated in GC cells and tissue. Data analyses indicated that ZEB1-AS1 and miR-149-3p are associated with the independent diagnosis and prognosis of GC. Functional assays support the theory that miR-149-3p hinders GC proliferation, migration and invasion, whereas its overexpression abrogates the corresponding effects induced by ZEB1-AS1. Lastly, dissection of the molecular mechanisms involved indicated that ZEB1-AS1 can regulate GC partly via a ZEB1-AS1/miR-149-3p axis. CONCLUSIONS: ZEB1-AS1 can interact with specific miRNAs, forming a miRNA-mediated ceRNA network and promoting GC progress, partly through a ZEB1-AS1/miR-149-3p axis.

miR-1236-3p inhibits invasion and metastasis in gastric cancer by targeting MTA2.

BACKGROUND: MicroRNAs deregulation are common in human tumor progression. miR-1236-3p has been reported to function as tumor suppressor microRNA in various malignancies. The aim of this study was to demonstrate the downregulated expression of miR-1236-3p in gastric cancer (GC) tissues and cell lines, and clarify its biological function in GC. METHODS: Real-time polymerase chain reaction was used to measure the mRNA level of miR-1236-3p in GC. Dual luciferase assay was used to demonstrate that MTA2 was one of the candidate target genes of miR-1236-3p. Western blots were utilized to detect the protein levels. Cell function assays were also performed to determine the function of miR-1236-3p in GC. RESULTS: miR-1236-3p expression, which was associated with lymph node metastasis, differentiation and clinical stage, was significantly reduced in GC tissues and cell lines. miR-1236-3p over-expression could inhibit GC cell proliferation, migration and invasion, and inhibition of miR-1236-3p expression had opposite effects. Furthermore, we demonstrated that MTA2 was a candidate target of miR-1236-3p, and miR-1236-3p over-expression significantly inhibited the process of epithelial-mesenchymal transition. We also found that miR-1236-3p could suppress the PI3K/Akt signaling pathway in GC cells. CONCLUSIONS: Our results suggest that miR-1236-3p functions as a tumor suppressor in GC and could be a promising therapeutic target for GC.

Expression of miR-634 in gastric carcinoma and its effects on proliferation, migration, and invasion of gastric cancer cells.

This study aims to observe the expression of microRNA (miR)-634 in different gastric cancer cell lines and tissues, and to study the effects of miR-634 on the proliferation, migration, and invasion of the gastric cancer cells. The miR-634 mimics and miR-634 inhibitors were transfected by lentivirus into human gastric cancer SGC-7901 and MGC-803 cells, and the miR-634 cells without transfection were used as the control group (NC group). The expression of miR-634 in the transfected cells was detected by qRT-PCR. Cell viability was measured by the CCK8 assay. The migration and invasion ability of the cells were detected by scratch assays and Transwell® chamber assays, respectively, and the luciferase assay verified the binding of miR-634 to the target gene JAG1. The expression level of miR-634 in gastric cancer tissues and cell lines was significantly lower than that in normal adjacent tissues and control cells. The survival of cells was significantly decreased, and number of cells migrating and invading was decreased in the miR-634 mimics group. However, in the miR-634 inhibitor group, the opposite results were observed. Over-expression of miR-634 inhibited the proliferation, migration, and invasion of gastric cancer cell lines, and the miR-634 target gene was JAG1.

MicroRNA-497 acts as a tumor suppressor in gastric cancer and is downregulated by DNA methylation.

Gastric cancer (GC) is one of the most common malignant tumors in the world and microRNAs (miRNAs) play an important role in GC. In this study, we found miR­497 played an important role and served as a novel biomarker in GC. Quantitative real-time PCR (qRT-PCR) was used to measure the miR­497 expression in GC cell lines and 86 paired GC samples and we also analyzed its correlation with GC clinicopathological parameters. A series of cellular function experiments were applied to validate the effects of miR­497 on GC. In addition, methylation-specific PCR (MSP) was applied to detect the gene methylation status. Finally, the correlation between miR­497 and the target gene was analyzed by western blotting assay. miR­497 was reduced obviously in GC cells and tissues and significantly associated with the pathologic stage. Low expression of miR­497 significantly inhibited the proliferation, invasion and migration of GC cell lines and accelerated apoptosis. Moreover, we found that the aberrant expression of miR­497 may be ascribed to DNA methylation. microRNA.org and luciferase reporter assay suggested that RAF1 was a direct target of miR­497 in GC. This study suggested that miR­497 could serve as a tumor suppressor and a potential early diagnostic marker of GC by targeting Raf-1 proto-oncogene, serine/threonine kinase (RAF1).