Demantmercer7575

However, only FZR1 was validated to be overexpressed in lung tissues of COPD with LUAD and cigarette smoke extract-stimulated A549 cells, a human LUAD cell line.

This study suggests overexpression of FZR1 may play a key role in the tumorigenesis of LUAD in patients with COPD.

This study suggests overexpression of FZR1 may play a key role in the tumorigenesis of LUAD in patients with COPD.

Endocrine therapy is the backbone therapy in estrogen receptor α (ER)-positive breast cancer, and tamoxifen resistance is a great challenge for endocrine therapy. Tamoxifen-resistant and sensitive samples from the international public repository, the Gene Expression Omnibus (GEO) database, were used to identify therapeutic biomarkers associated with tamoxifen resistance.

In this study, integrated analysis was used to identify tamoxifen resistance-associated genes. Differentially expressed genes (DEGs) were identified. Gene ontology and pathway analysis were then analyzed. Weighted correlation network analysis (WGCNA) was performed to find modules correlated with tamoxifen resistance. Protein-protein interaction (PPI) network was used to find hub genes. Genes of prognostic significance were further validated in another GEO dataset and cohort from Shanghai Ruijin Hospital using RT-PCR.

A total of 441 genes were down-regulated and 123 genes were up-regulated in tamoxifen-resistant samples. Those up-regulat resistance, and high expression of these genes could predict poor prognosis of patients receiving tamoxifen. These genes may be potential targets to improve efficacy of endocrine therapy in breast cancer, and inhibitors targeted these genes could be used in endocrine-resistant patients.

Doxorubicin (Dox) resistance is a primary obstacle for the treatment of osteosarcoma. Meanwhile, β-Elemene was shown to exhibit an anti-proliferative effect on osteosarcoma cells. However, the role of a combination of Dox with β-Elemene on osteosarcoma cells remains unclear. Thus, this study aimed to investigate the role of the combination of Dox with β-Elemene on the proliferation, apoptosis and oxidative stress of Dox-resistance osteosarcoma cells.

CKC-8, EdU staining and flow cytometry assays were used to determine the viability, proliferation and apoptosis of Dox-resistance osteosarcoma cells, respectively. Meanwhile, the expression of antioxidant protein peroxiredoxin-1 (Prx-1) in Dox-resistance osteosarcoma cells was detected with Western blot assay.

In this study, the inhibitory effects of Dox on the viability and proliferation of Dox-resistance osteosarcoma cells were significantly enhanced by β-Elemene. In addition, the combination of Dox and β-Elemene markedly induced the apoptosis and oxidative stress in Dox-resistance osteosarcoma cells. Moreover, combination treatment notably downregulated the expression of Prx-1 in Dox-resistance osteosarcoma cells, indicating that combination treatment inhibited the antioxidant capacity of Dox-resistance osteosarcoma cells. In vivo experiments confirmed that β-Elemene could enhance the anti-tumor effect of Dox in Saos-2/Dox xenograft model.

We found that β-Elemene could reverse Dox resistance in Dox-resistance osteosarcoma cells via inhibition of Prx-1. Therefore, combining Dox with β-Elemene might be considered as a therapeutic approach for the treatment of Dox-resistant osteosarcoma.

We found that β-Elemene could reverse Dox resistance in Dox-resistance osteosarcoma cells via inhibition of Prx-1. Therefore, combining Dox with β-Elemene might be considered as a therapeutic approach for the treatment of Dox-resistant osteosarcoma.[This retracts the article DOI 10.2147/OTT.S156810.].

Integrin alpha 2 (ITGA2) is highly expressed in various cancers. ITGA2 up regulation promotes tumor proliferation, invasion, migration, and angiogenesis and ITGA2 is a poor prognostic factor in many tumors. However, the mechanism underlying its role in esophageal squamous cell carcinoma (ESCC) is unknown.

The expression profile of ITGA2 in ESCC was analyzed using the Gene expression profiling interactive analysis (GEPIA). ESCC tissues were analyzed by real time PCR (RT-qPCR) and immunohistochemistry to verify ITGA2 expression. find more The impact of ITGA2 on the clinicopathological characteristics was explored using a chi-square test. Apoptosis, Transwell, colony formation, and wound healing assays were conducted to characterize the roles of ITGA2 in ESCC. Its impact on tumorigenesis was further examined using a tumor xenograft model. The expression of proteins associated with the epithelial-mesenchymal Transition (EMT) and focal adhesion kinase (FAK)/AKT pathway and regulated by ITGA2 was evaluated with Western bon, invasion and migration, while inhibiting apoptosis and promoting EMT in ESCC, possibly via FAK/AKT phosphorylation. These findings highlight the therapeutic value of ITGA2 in ESCC.

Primary pancreatic mucoepidermoid carcinoma (MEC) is an extremely rare malignant tumor with unclear etiology and pathogenesis. There are only eleven reported cases in English papers published from 1959 to 2020. MEC generally occurs in the salivary gland, but cases in the pancreas have also been reported. Although being considered as a low-grade indolent carcinoma, pancreatic MEC always invades the surrounding lymph node and metastasizes. The prognosis of pancreatic MEC is unsatisfactory. To date,the genetic alterations, mechanistic relationships among mutated genes and signaling pathways of pancreatic MEC are unclear.

This paper presents a case of rare primary pancreatic MEC in a 56-year-old male patient with liver metastasis. Radical surgery of distal pancreatectomy and radiofrequency ablation (RFA) of two liver metastatic lesions is conducted. Targeted-gene sequencing and bioinformatics analysis tools, including STRING, DAVID, cBioPortal, DGidb and Human Protein Atlas database (HPA), are used to clarifylecular alterations, functional information and enrichment pathway.

Pancreatic MEC requires early and effective treatment, and lymph node metastases and multiple organ metastases were unfavorable prognostic factors. Pancreatic MEC can be compared with other pancreatic cancers that have characteristic clinical phenotype, molecular alterations, functional information and enrichment pathway.