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Background Long noncoding RNA ANRIL has been found to be involved in the pathogenesis of diabetic kidney disease (DKD) and is expected to be a new target for prevention of DKD. However, the circulating expression and clinical significance of ANRIL in DKD patients is uncertain. This study aims to explore this issue. Methods The study consisted of 20 healthy controls, 22 T2DM patients (normalbuminuria) and 66 DKD patients (grouped as follows: microalbuminuria, n = 23; macroalbuminuria, n = 22 and renal dysfunction, n = 21). The expressions of ANRIL in peripheral whole blood of all participants were measured by RT-qPCR. Results The expression of ANRIL was significantly up-regulated in DKD patients (microalbuminuria, macroalbuminuria and renal dysfunction groups) than that in healthy control group. ANRIL was also over-expressed in macroalbuminuria and renal dysfunction groups in comparison with normalbuminuria group. ANRIL expression was positively correlated with Scr, BUN, CysC, urine β2-MG and urine α1-MG; while negatively correlated with eGFR in DKD patients. In addition, ANRIL was the risk factor for DKD with OR value of 1.681. The AUC of ANRIL in identifying DKD was 0.922, and the sensitivity and specificity of DKD diagnosis were 83.3% and 90.5%, respectively. Conclusion Our results indicated that highly expressed ANRIL in peripheral blood is associated with progression of DKD. Circulating ANRIL is an independent risk factor of DKD and has a highly predictive value in identifying DKD.

Tripartite motif containing-21 (TRIM21), an E3 ubiquitin ligase, was initially found to be involved in antiviral responses and autoimmune diseases. Recently studies have reported that TRIM21 plays a dual role in cancer promoting and suppressing in the occurrence and development of various cancers. Despite the fact that TRIM21 has effects on multiple metabolic processes, inflammatory responses and the efficacy of tumor therapy, there has been no systematic review of these topics. Herein, we discuss the emerging role and function of TRIM21 in cancer metabolism, immunity, especially the immune response to inflammation associated with tumorigenesis, and also the cancer treatment, hoping to shine a light on the great potential of targeting TRIM21 as a therapeutic target.

Tripartite motif-containing 21 (TRIM21) has been reported to have a cancer-promoting or anticancer effect in various tumors; however, its role in ovarian cancer (OC) remains to be elucidated. In this study, we explored the biological function of TRIM21 in OC progression and investigated the potential mechanisms. We found that TRIM21 was remarkably decreased in OC tissues and cell lines compared with adjacent-cancerous tissues and normal ovarian epithelium cell. Decreased expression of TRIM21 in OC patients was significantly correlated with shorter overall and disease-specific survival by The Cancer Genome Atlas database (TCGA) analysis. Functional assays revealed that TRIM21 inhibited the migration and invasion of OC cells; and that TRIM21 also obviously impaired cell proliferation by inhibiting cell cycle progression

Protein arginine methyltransferase 1 (PRMT1) is able to promote breast cancer cell proliferation. However, the detailed mechanisms of PRMT1-mediated breast cancer cell proliferation are largely unknown. In this study, we reveal that PRMT1-mediated methylation of EZH2 at the R342 site (meR342-EZH2) has a great effect on PRMT1-induced cell proliferation. We also demonstrate that meR342-EZH2 can accelerate breast cancer cell proliferation in vitro and in vivo. Further, we show that meR342-EZH2 promotes cell cycle progression by repressing P16 and P21 transcription expression. In terms of mechanism, we illustrate that meR342-EZH2 facilitates EZH2 binding with SUZ12 and PRC2 assembly by preventing AMPKα1-mediated phosphorylation of pT311-EZH2, which results in suppression of P16 and P21 transcription by enhancing EZH2 expression and H3K27me3 enrichment at P16 and P21 promoters. Finally, we validate that the expression of PRMT1 and meR342-EZH2 is negatively correlated with pT311-EZH2 expression. Our findings suggest that meR342-EZH2 may become a novel therapeutic target for the treatment of breast cancer.

Tripartite motif-containing 21 (Trim21) is mainly involved in antiviral responses and autoimmune diseases. Although Trim21 has been reported to have a cancer-promoting or anticancer effect in various tumours, its role in renal cell cancer (RCC) remains to be elucidated. In this study, we demonstrate that Trim21 is downregulated in primary RCC tissues. Low Trim21 expression in RCC is correlated with poor clinicopathological characteristics and short overall survival. Moreover, we illustrate that Trim21 inhibits RCC cells glycolysis through the ubiquitination-mediated degradation of HIF-1α, which inhibits the proliferation, tumorigenesis, migration, and metastasis of RCC cells in vitro and in vivo. Our findings show that Trim21 may become a promising predictive biomarker for the prognosis of patients with RCC.

Tumor-associated macrophages (TAMs) are important monocytes in the breast cancer microenvironment. They facilitate the distant metastasis of breast cancer. However, the detailed mechanisms of TAM-derived cancer metastasis have not been clearly elucidated. Here, we demonstrate that PRMT1 is essential for TAM-mediated breast cancer cell migration and metastasis. TAMs increase EZH2 stability by stimulating PRMT1-mediated meR342-EZH2 formation through the secretion of interleukin-6 (IL-6) cytokine. Moreover, high expression levels of TAMs are positively correlated with PRMT1, meR342-EZH2, and EZH2 expression in breast cancer patients. Our study presents a novel mechanism of TAM-induced breast cancer metastasis via the IL-6-PRMT1-meR342-EZH2 axis.

The treatment of cancer has made great progress. However, drug resistance remains problematic. Multiple physiologic processes of tumor development can be dominated by central and sympathetic nervous systems. The interactions between the nervous system, immune system, and tumor occur consistently and dynamically. Recent evidence suggests that nerves and neural signals are intimately involved in the development of resistance to cancer therapies. In this review, we will provide an overview of the recent progress in this rapidly growing area and discuss the potential new strategies for targeting the neural signaling pathway to improve the effectiveness of chemotherapies, targeted therapies, and immunotherapies.

Background Traditional Chinese medicine (TCM) is a highly important complement to modern medicine and is widely practiced in China and in many other countries. The work of Chinese medicine is subject to the two factors of the inheritance and development of clinical experience of famous Chinese medicine practitioners and the difficulty in improving the service capacity of basic Chinese medicine practitioners. Heterogeneous information networks (HINs) are a kind of graphical model for integrating and modeling real-world information. Through HINs, we can integrate and model the large-scale heterogeneous TCM data into structured graph data and use this as a basis for analysis. Methods Mining categorizations from TCM data is an important task for precision medicine. In this paper, we propose a novel structured learning model to solve the problem of formula regularity, a pivotal task in prescription optimization. We integrate clustering with ranking in a heterogeneous information network. Results The results from experiments on the Pharmacopoeia of the People’s Republic of China (ChP) demonstrate the effectiveness and accuracy of the proposed model for discovering useful categorizations of formulas. Conclusions We use heterogeneous information networks to model TCM data and propose a TCM-HIN. Combining the heterogeneous graph with the probability graph, we proposed the TCM-Clus algorithm, which combines clustering with ranking and classifies traditional Chinese medicine prescriptions. The results of the categorizations can help Chinese medicine practitioners to make clinical decision.

Proinflammatory macrophage (M1) is now being suggested as a potential therapeutic strategy for cancer because of its tumoricidal capacity. However, few studies have been focused directly on the effects of M1 macrophages on cancer cells. Here, we found that M1 induced a subpopulation of CD44high/CD24-/low or ALDH1+ cells with CSC-like phenotypes from different types of breast cancer cells (BCCs) in a paracrine manner. Stat3/NF-κB pathways in BCCs were activated by proinflammatory cytokines, igniting Lin-28B-let-7-HMGA2 axis to induce CSC through epithelial-mesenchymal transition (EMT). Previously, we reported that Stat3-coordinated Lin-28B-let-7-HMGA2 axis initiated EMT in BCCs. Here, inhibition of Stat3/NF-κB pathways or Lin-28B-let-7-HMGA2 axis suppressed EMT/CSCs program. Notably, HMGA2 knockdown directly repressed M1-induced CSC formation and expression of Klf-4 and Nanog. Meanwhile, prolonged coculture with BCCs endowed M1 with M2 properties. M1 supernatant induced CSC from non-stem cancer cells, while M2 supernatant sustained a higher proportion of ALDH1+ cells. Our data suggest that macrophages might modulate CSC formation and maintenance by transferring between M1/M2 phenotype. Given that M1 are being considered as a promising immunotherapy tool, it is important to inhibit their CSC-inducing potential by targeting key molecules and pathways.