Now days, obesity is a major risk factor for intervertebral disc degeneration (IDD). However, adipokine, such as chemerin is a novel cytokine, which is secreted by adipose tissue, and are thought to be played major roles in various degenerative diseases. Obese individuals are known to have high concentration of serum chemerin. Our purpose was to study whether chemerin acts as a biochemical relationship between obesity, and IDD. In this study, we found that the expression level of chemerin was significantly increased in the human degenerated nucleus pulposus (NP) tissues, and had higher level in the obese people than the normal people. Chemerin significantly increased the inflammatory mediator level, contributing to ECM degradation in nucleus pulposus cells (NPCs). Furthermore, chemerin overexpression aggravates the puncture-induced IVDD progression in rats, while knockdown CMKLR1 reverses IVDD progression. Chemerin activates the NF-kB signaling pathway via its receptors CMKLR1, and TLR4 to release inflammatory mediators, which cause matrix degradation, and cell aging. These findings generally provide novel evidence supporting the causative role of obesity in IDD, which is essentially important to literally develop novel preventative or generally therapeutic treatment in the disc degenerative disorders.

Colorectal cancer (CRC) is a solid tumor with high morbidity and mortality rates. Accumulating evidence shows that the soluble carrier family 35 member A2 (SLC35A2), a nucleotide sugar transporter, plays a key role in the pathogenesis of various tumors. However, its expression and function in CRC has not been fully elucidated.

Uveal melanoma is a highly malignant tumor in the eye. Its recurrence and metastasis are common, and the prognosis is poor.

Currently, the role of liquid-liquid phase separation (LLPS) in cancer has been preliminarily explained. However, the significance of LLPS in breast cancer is unclear. In this study, single cell sequencing datasets GSE188600 and GSE198745 for breast cancer were downloaded from the GEO database. Transcriptome sequencing data for breast cancer were downloaded from UCSC database. We divided breast cancer cells into high-LLPS group and low-LLPS group by down dimension clustering analysis of single-cell sequencing data set, and obtained differentially expressed genes between the two groups. Subsequently, weighted co-expression network analysis (WGCNA) was performed on transcriptome sequencing data, and the module genes most associated with LLPS were obtained. COX regression and Lasso regression were performed and the prognostic model was constructed. Subsequently, survival analysis, principal component analysis, clinical correlation analysis, and nomogram construction were used to evaluate the significance of the prognostic model. Finally, cell experiments were used to verify the function of the model's key gene, PGAM1. We constructed a LLPS-related prognosis model consisting of nine genes: POLR3GL, PLAT, NDRG1, HMGB3, HSPH1, PSMD7, PDCD2, NONO and PGAM1. By calculating LLPS-related risk scores, breast cancer patients could be divided into high-risk and low-risk groups, with the high-risk group having a significantly worse prognosis. Cell experiments showed that the activity, proliferation, invasion and healing ability of breast cancer cell lines were significantly decreased after knockdown of the key gene PGAM1 in the model. Our study provides a new idea for prognostic stratification of breast cancer and provides a novel marker: PGAM1.

Hepatocellular carcinoma (HCC) is one of the most common cancers in the world and is often associated with a poor prognosis. The main reason for this poor prognosis is that inconspicuous early symptoms lead to delayed diagnosis. Treatment options for advanced HCC remain limited and ineffective. In this context, the exploration of the immune microenvironment in HCC becomes attractive. In this study, we divided HCC into immune cell and non-immune cell subtypes, by single-cell sequencing analysis of GEO dataset GSE146115. We found differentially expressed genes in the two subtypes, which we used to construct a prognostic model for HCC through Cox and Lasso regressions. Our prognostic model can accurately evaluate the prognosis of HCC patients, and provide a reference for the design of immunotherapy for HCC.

The goal of the study is to assess the clinical value and the potential mechanism of SLC12A9 combing transcriptome and single cell sequencing data.

At present, cancer is still one of the principal diseases to represent a serious danger to human health. Although research on the pathogenesis and treatment of cancer is progressing rapidly, the current knowledge on this topic is far from sufficient. Some tumors with poor prognoses lack effective prognostic biomarkers.

RecQ mediated genome instability 2 (RMI2) is an essential component of the BLM-TopoIIIa-RMI1-RMI2 (BTR) complex. However, the mysterious veil of the potential immunological relationship of RMI2 in tumorigenesis and development has not been revealed.

We investigated the role of long non-coding RNA (lncRNA) LOC146880 in esophageal squamous cell carcinoma (ESCC). LOC146880 was significantly upregulated in ESCC tissues (n = 21) and cell lines compared to the corresponding controls. Higher LOC146880 expression correlated with poorer overall survival (OS) of ESCC patients. Moreover, CREB-binding protein (CBP) and H3K27 acetylation levels were significantly higher in the LOC146880 promoter in ESCC cell lines than in the controls. LOC146880 silencing inhibited in vitro proliferation, invasion, migration, and epithelial-mesenchymal transition of ESCC cells. LOC146880 silencing also induced G1-phase cell cycle arrest and apoptosis in ESCC cells. Bioinformatics analysis, dual luciferase reporter assays, and RNA immunoprecipitation assays showed that LOC146880 regulates FSCN1 expression in ESCC cells by sponging miR-328-5p. Moreover, FSCN1 expression correlated with activation of the MAPK signaling pathway in ESCC cells and tissues. In vivo xenograft tumor volume and liver metastasis were significantly reduced in nude mice injected with LOC146880-silenced ESCC cells as compared to those injected with control shRNA-transfected ESCC cells. These findings show that the LOC146880/miR-328-5p/FSCN1/MAPK axis regulates ESCC progression in vitro and in vivo. LOC146880 is thus a promising prognostic biomarker and potential therapeutic target in ESCC.

Clear cell renal cell carcinoma (ccRCC) is a heterogeneous tumor that the underlying molecular mechanisms are largely unclear. This study aimed to elucidate the key candidate genes and pathways in ccRCC by integrated bioinformatics analysis. 1387 differentially expressed genes were identified based on three expression profile datasets, including 673 upregulated genes and 714 downregulated genes. Then we used weighted correlation network analysis to identify 6 modules associated with pathological stage and grade, blue module was the most relevant module. GO and KEGG pathway analyses showed that genes in blue module were enriched in cell cycle and metabolic related pathways. Further, 25 hub genes in blue module were identified as hub genes. Based on GEPIA database, 9 genes were associated with progression and prognosis of ccRCC patients, including PTTG1, RRM2, TOP2A, UHRF1, CEP55, BIRC5, UBE2C, FOXM1 and CDC20. Then multivariate Cox regression showed that the risk score base on 9 key genes signature was a clinically independent prognostic factor for ccRCC patients. Moreover, we screened out several new small molecule drugs that have the potential to treat ccRCC. Few of them were identified as biomarkers in ccRCC. In conclusion, our research identified 9 potential prognostic genes and several candidate small molecule drugs for ccRCC treatment.

Gastric cancer is a prevalent type of tumor with a poor prognosis. Given the high occurrence of genomic instability in gastric cancer, it is essential to investigate the prognostic significance of genes associated with genomic instability in this disease.