First-principles study of the electronic structures and optical properties of g-ZnO/CdX (X = S, Se, Te) van der Waals heterostructures.

The stability, electronic structures and optical properties of g-ZnO/CdX (X = S, Se, Te) heterostructures are studied by density functional theory. It is found that the stable monolayers spacing of the corresponding heterostructure decreases with the increase of the X atomic radius in the CdX monolayers. The constructed g-ZnO/CdX heterostructures all belong to direct band gap, 2.12 eV, 2.09 eV and 1.99 eV, respectively. Electrostatic potential results show that the two monolayers form an internal electric field at the heterostructure interface, and can inhibit the recombination of photogenerated electron hole pairs, and effectively extend the carrier lifetime. Charge density difference analysis shows that charge redistribution mainly occurs in the interfacial region. The optical properties show that the absorption of g-ZnO in the visible range is achieved by heterostructure. In general, with the smallest band gap and the strongest built-in electric field, g-ZnO/CdTe could have the best carrier separation efficiency. And the optical property analysis proves that the g-ZnO/CdTe heterostructure system has the highest utilization ratio of visible light. The above results show that the electronic structure and optical properties of g-ZnO/CdTe heterostructure are the best, and it can be inferred that this heterostructure will be the most beneficial to improve the photocatalytic activity of g-ZnO, providing a new direction for its application in the field of photocatalysis.

STAMBPL1 promotes breast cancer cell resistance to cisplatin partially by stabilizing MKP-1 expression.

Dual-specificity mitogen-activated protein kinase phosphatase-1 (MKP-1/DUSP1/CL-100) has been documented to promote breast cancer cell survival and chemoresistance. MKP-1 is an unstable protein that is ubiquitinated and degraded via the ubiquitin-proteasome system. However, it is not clear how MKP-1 protein stability is regulated in breast cancer. In this study, we performed a genome-wide siRNA library screen of deubiquitinases (DUBs) and identified STAMBPL1 as an MKP-1 DUB in breast cancer cells. STAMBPL1 interacts with MKP-1 and stabilizes MKP-1 via deubiquitination. Both STAMBPL1 and MKP-1 depletion sensitize breast cancer cells to cisplatin in vitro and in vivo, and ectopic overexpression of MKP-1 partially rescues STAMBPL1 depletion-induced cisplatin sensitivity. Furthermore, STAMBPL1 and MKP-1 depletion increased breast cancer sensitivity to cisplatin by increasing the phosphorylation and activation of c-Jun N-terminal protein kinase (JNK). Collectively, our findings not only identify STAMBPL1 as an MKP-1 DUB but also reveal a critical mechanism that regulates MKP-1 expression in breast cancer. Our findings indicate that the STAMBPL1/MKP-1 axis represents a potential therapeutic target in breast cancer.

Analysis of the Prognostic Value and Gene Expression Mechanism of SHOX2 in Lung Adenocarcinoma.

Background: Detection of SHOX2 methylation has been used to assist in the early diagnosis of lung cancer in many hospitals as SHOX2 may be important in the tumorigenesis of lung cancer. However, there are few studies on the mRNA expression, methylation, and molecular mechanism of SHOX2 in lung cancer. We aimed to explore the role of SHOX2 in lung adenocarcinoma (LUAD). Methods: First, we examined the differential expression of SHOX2 mRNA and methylation in cancerous and normal tissues using databases. Second, we analyzed the relationship between SHOX2 expression and common clinical parameters in LUAD patients. Third, we further explored the methylated level and its specific location of SHOX2 and the mainly factors of SHOX2 gene expression. Finally, we screened the correlatively expressed genes to analyze the pathways from the Gene Ontology and Kyoto Encyclopedia of Genes and Genomes using DAVID. Results: We found that the mRNA expression of SHOX2 was higher in multiple cancers, including LUAD and lung squamous cell carcinoma (LUSC), than in normal tissues. Among LUAD patients, SHOX2 expression was higher in patients of middle-young age, with smoking history, in advanced stages, and with nodal distant metastasis. In addition, our results showed that patients with high expression of SHOX2 are prone to recurrence, poor differentiation, and poor prognosis. Thus, we identified that SHOX2 might be an oncogene for LUAD progression. The main factor influencing the high expression of SHOX2 mRNA may be DNA methylation, followed by copy number variation (CNV), but not by gene mutations in LUAD. Unexpectedly, we found that SHOX2 undergoes hypomethylation in the gene body instead of hypermethylation in the promoter. Additionally, SHOX2 has cross talk in the PI3K-Akt signaling pathway and ECM-receptor interaction. Conclusion: SHOX2 is highly expressed in most cancers. SHOX2 gene expression might be mainly regulated by methylation of its gene body in LUAD, and its high expression or hypomethylation indicates poor differentiation and poor prognosis. SHOX2 could be involved in PI3K-Akt and other important cancer-related signaling pathways to promote tumorigenesis.