The deubiquitinase enzyme RPN11 is involved in oncogenesis in various types of cancer. However, in breast cancer, the expression levels, prognostic relevance and biological function of RPN11 remains unclear. In the present study, RPN11 expression levels in breast cancer tissues and adjacent non‑tumor tissues were determined by reverse transcription‑quantitative polymerase chain reaction and immunohistochemical staining, and the association of RPN11 with clinicopathological features of breast cancer was evaluated. RPN11 expression was upregulated in breast cancer tissues compared with healthy tissues. Additionally, high expression levels of RPN11 may be an indicator of poor prognosis, as validated by a breast cancer cohort from the Gene Expression Omnibus database. Knockdown of RPN11 in MDA‑MB‑231 and T47D cells significantly reduced cell proliferation and enhanced G0/G1 arrest and apoptosis. Exogenous overexpression of RPN11 in MCF7 and Hs578T cells promoted cell growth and inhibited apoptosis. In addition, knockdown of RPN11 abrogated cell migration and reduced epithelial‑mesenchymal transition. In conclusion, these findings suggested that RPN11 may function as an oncogene and its upregulation in breast cancer suggests that it may be a therapeutic target.

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Lymph node metastasis is a major prognostic factor for patients with breast cancer.

Macrophages are key innate immune cells in the tumor microenvironment that regulate primary tumor growth, vascularization, metastatic spread and response to therapies. Macrophages can polarize into two different states (M1 and M2) with distinct phenotypes and functions. To investigate the known tumoricidal effects of M1 macrophages, we obtained RNA expression profiles and clinical data from The Cancer Genome Atlas Thyroid Cancer (TCGA-THCA). The proportions of immune cells in tumor samples were assessed using CIBERSORT, and weighted gene co-expression network analysis (WGCNA) was used to identify M1 macrophage-related modules. Univariate Cox analysis and LASSO-Cox regression analysis were performed, and four genes (SPP1, DHRS3, SLC11A1, and CFB) with significant differential expression were selected through GEPIA. These four genes can be considered hub genes. The four-gene risk-scoring model may be an independent prognostic factor for THCA patients. The validation cohort and the entire cohort confirmed the results. Univariate and multivariate Cox analysis was performed to identify independent prognostic factors for THCA. Finally, a prognostic nomogram was built based on the entire cohort, and the nomogram combining the risk score and clinical prognostic factors was superior to the nomogram with individual clinical prognostic factors in predicting overall survival. Time-dependent ROC curves and DCA confirmed that the combined nomogram is useful. Gene set enrichment analysis (GSEA) was used to elucidate the potential molecular functions of the high-risk group. Our study identified four genes associated with M1 macrophages and established a prognostic nomogram that predicts overall survival for patients with THCA, which may help determine clinical treatment options for different patients.

Background Thyroid cancer causes considerable mortality and morbidity across the globe. Owing to the unavailability of biomarkers and the adverse effects of existing drugs, there is an urgent need to develop efficient chemotherapy for the treatment of thyroid cancers. Plants have served as exceptional source of drugs for the treatment of lethal diseases. The purpose of this study was to evaluate the anticancer effects of ferruginol against thyroid cancer cells. Material/Methods We monitored the cell proliferation rate using 3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was detected using 4′,6-diamidino-2-phenylindole (DAPI), acridine orange/ethidium bromide (AO/EB), and annexin V/propidium iodide (PI) staining. Reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) levels were examined by fluorescence microscopy. Protein expressed was examined by western blotting. Results We found that ferruginol exerted potent antiproliferative action against thyroid cancer cells, and an IC 50 of 12 μM was observed for ferruginol against the MDA-T32 cell line. The toxic effects of ferruginol were less pronounced against normal cells. The anticancer effects of ferruginol were likely due to the induction of apoptosis which was also associated with upregulation of Bax and downregulation of Bcl-2. Ferruginol also caused ROS mediated alterations in the MMP of MDA-T32 cells. In MDA-T32 cells, ferruginol might also block the MAPK and PI3K/AKT signaling pathway, which is believed to be an important therapeutic target of anticancer drugs. Conclusions In conclusion, in view of the results of this study, it might be suggested that ferruginol might serve as an essential lead molecule for the treatment of thyroid cancer provided further in-depth studies especially studying ferruginol toxicological as well as in vivo studies are needed.

This research was conducted to study the effects of dietary inclusion of mulberry leaf powder (MLP) on growth performance, meat quality, antioxidant activity, and carcass traits of Tibetan pigs. Eighteen Tibetan pigs (33.8 ± 1.1 kg) were assigned to two treatment groups randomly and received either the control diet (CON) or a basal diet containing 8% MLP (MLP) for two months. After the two-month feeding trial, the MLP group showed lower backfat thickness while a higher lean percentage. Compared with CON pigs, MLP pigs had higher serum CAT activity. In addition, dietary MLP supplementation significantly decreased the muscle shear force. Muscle fiber morphology analysis showed that MLP pigs had larger muscle fiber density while smaller muscle fiber cross-sectional area. Up-regulated gene expression of myosin heavy chain (MyHC)IIa was also observed in MLP pigs. These results indicate that the enhanced antioxidant activity and altered muscle fiber type and morphology appeared to contribute to the improvement of meat quality in Tibetan pigs fed diets containing MLP.

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Papillary thyroid cancer (PTC) is one of the most common malignant tumors in female, and estrogen can affect its progression. However, the targets and mechanisms of estrogen action in PTC remain unclear. Therefore, this study focuses on the relationship between estrogen-related genes (ERGs) expression and prognosis in PTC, particularly neuropeptide U (NMU), and its important role in tumor progression. Based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases, differentially expressed genes (DEGs) predominantly enriched in ERGs were identified between PTC and normal tissue. Then, we identified ERGs that contributed most to PTC prognosis, including Transducer of ERBB2 1 (TOB1), trefoil factor 1 (TFF1), phospholipase A and acyltransferase 3 (PLAAT3), NMU, kinesin family member 20A (KIF20A), DNA topoisomerase II alpha (TOP2A), tetraspanin 13 (TSPAN13), and carboxypeptidase E (CPE). In addition, we confirmed that NMU was highly expressed in PTC and explored the effect of NMU on PTC cells proliferation in vitro and in vivo . The results showed that the proliferative capacity of PTC cells was significantly reduced with NMU knockdown. Moreover, the phosphorylation levels of the Kirsten rat sarcoma virus (KRAS) signaling pathway were significantly lower with NMU knockdown. These results suggest that ERGs, especially NMU, may be novel prognostic indicators in PTC.