analysis-based-on-tcga-data-single-cell-data-taking-trpm4-as-an

Analysis Based on TCGA Data and Single-cell Data, taking <em>TRPM4</em> as an Example

In this article, an analysis method is introduced based on public transcriptomic datasets and single-cell datasets, which could be used to comprehensively ...

Nanjing Medical University

The role of radio frequency ablation (RFA) in small renal tumors remains controversial. This systematic review was performed to compare clinical outcomes of RFA versus partial nephrectomy (PN) for the treatment of T1 renal tumors.

Comparative outcomes of radio frequency ablation versus partial nephrectomy for T1 renal tumors: a systematic review.

Extensive research has revealed the pivotal role of kinesin family member 20A (KIF20A) in cancer. However, its latent involvement in renal clear cell carcinoma (ccRCC) still remains unclear. Thus, here we explored the role of KIF20A in ccRCC. For this, a series of software including R (v. 3.6.1), SPSS (v. 23), ImageJ and FlowJo were used for the analyses. Open-access data were obtained from The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC) and Gene Expression Omnibus (GEO) databases. Weighted Gene Co-expression Network Analysis (WGCNA) was used for module gene identification. In vitro results indicated that KIF20A expression is up-regulated in ccRCC tissue. KIF20A knockdown was able to inhibite cell proliferation and invasion of kidney A498 and Caki-1 cells. Meanwhile, KIF20A showed a strong association with immune infiltration. Particularly, KIF20A had a strong positive correlation with Th2 cells, Treg cells and Macrophages, but a negative correlation with Th17 cells, Mast cells and NK cells. These correlations may suggest the use of KIF20A as an underlying immunotherapy target in ccRCC. Our data indicated that KIF20A may promote cell invasion and proliferation in ccRCC, thus serving as an independent tumor marker and a putative therapeutic target.

Upregulation of KIF20A promotes tumor proliferation and invasion in renal clear cell carcinoma and is associated with adverse clinical outcome.

LncRNAs play a pivotal role in tumorigenesis and development. However, the potential involvement of lncRNAs in colon adenocarcinoma (COAD) needs to be further explored. All the data used in this study were obtained from The Cancer Genome Atlas database, and all analyses were conducted using R software. Basing on the seven prognosis-related lncRNAs finally selected, we developed a prognosis-predicting model with powerful effectiveness (training cohort, 1 year: AUC = 0.70, 95% Cl = 0.57-0.78; 3 years: AUC = 0.71, 95% Cl = 0.6-0.8; 5 years: AUC = 0.76, 95% Cl = 0.66-0.87; validation cohort, 1 year: AUC = 0.70, 95% Cl = 0.58-0.8; 3 years: AUC = 0.73, 95% Cl = 0.63-0.82; 5 years: AUC = 0.68, 95% Cl = 0.5-0.85). The VEGF and Notch pathway were analyzed through GSEA analysis, and low immune and stromal scores were found in high-risk patients (immune score, cor =  - 0.15, P < 0.001; stromal score, cor =  - 0.18, P < 0.001) , which may partially explain the poor prognosis of patients in the high-risk group. We screened lncRNAs that are significantly associated with the survival of patients with COAD and possibly participate in autophagy regulation. This study may provide direction for future research.

Identification of novel autophagy-related lncRNAs associated with a poor prognosis of colon adenocarcinoma through bioinformatics analysis.

The cytosolic sulfotransferases (SULTs) are phase II conjugating enzymes, which are widely expressed in the liver and mainly mediate the sulfation of numerous xenobiotics and endogenous compounds. However, the role of various SULTs genes has not been reported in hepatocellular carcinoma (HCC). This study aims to analyze the expression and potential functional roles of SULTs genes in HCC and to identify the role of SULT2A1 in HCC stemness as well as the possible mechanism. We found that all of the 12 SULTs genes were differentially expressed in HCC. Moreover, clinicopathological features and survival rates were also investigated. Multivariate regression analysis showed that SULT2A1 and SULT1C2 could be used as independent prognostic factors in HCC. SULT1C4, SULT1E1, and SULT2A1 were significantly associated with immune infiltration. SULT2A1 deficiency in HCC promoted chemotherapy resistance and stemness maintenance. Mechanistically, silencing of SULT2A1 activated the AKT signaling pathway, on the one hand, promoted the expression of downstream stemness gene c-Myc, on the other hand, facilitated the NRF2 expression to reduce the accumulation of ROS, and jointly increased HCC stemness. Moreover, knockdown NR1I3 was involved in the transcriptional regulation of SULT2A1 in stemness maintenance. In addition, SULT2A1 knockdown HCC cells promoted the proliferation and activation of hepatic stellate cells (HSCs), thereby exerting a potential stroma remodeling effect. Our study revealed the expression and role of SULTs genes in HCC and identified the contribution of SULT2A1 to the initiation and progression of HCC.

An integrated investigation of sulfotransferases (SULTs) in hepatocellular carcinoma and identification of the role of SULT2A1 on stemness.

Ubiquitinases are known to catalyze ubiquitin chains on target proteins to regulate various physiological functions like cell proliferation, autophagy, apoptosis, and cell cycle progression. As a member of E3 ligase, ubiquitin protein ligase E3 component n-recognin 5 (UBR5) belongs to the HECT E3 ligase and has been reported to be correlated with various pathophysiological processes. In this review, the authors give a comprehensive insight into the structure and function of UBR5. The authors discuss the specific domains of UBR5 and explore their biological functions separately. Furthermore, the authors describe the involvement of UBR5 in different pathophysiological conditions, including immune response, virus infection, DNA damage response, and protein quality control. Moreover, the authors provide a thorough summary of the important roles and regulatory mechanisms of UBR5 in cancers and other diseases. On the whole, investigating the domains and functions of UBR5, elucidating the underlying mechanisms of UBR5 with various substrates in detail may provide new theoretical basis for the treatment of diseases, including cancers, which could improve future studies to construct novel UBR5-targeted therapy strategies.

A review: targeting UBR5 domains to mediate emerging roles and mechanisms - chance or necessity?

TRIM14 is an important member of the TRIM family and is widely expressed in a variety of tissues. Like other members of the TRIM family, TRIM14 is also involved in ubiquitination modifications. TRIM14 was initially reported as an interferon-stimulated gene (ISG). In recent years, many studies have focused on the regulatory role of TRIM14 in signaling pathways such as the PI3K/Akt, NF-κB, and cGAS/STING pathways and revealed its mechanism of action in a variety of pathophysiological processes, and the regulation of TRIM14 has attracted the interest of many researchers as a new direction for the treatment of various diseases. However, there are no reviews on the role of TRIM14 in diseases. In this paper, we will describe the structure of TRIM14, review its role in cancer, cardiovascular disease, cervical spondylosis, inflammation and antiviral immunity, and provide an outlook on future research directions.

Emerging discoveries on the role of TRIM14: from diseases to immune regulation.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely associated with insulin resistance (IR). However, the prognostic value of different alternative IR surrogates in patients with MASLD remains unclear. This study aimed to evaluate the association between various IR indices and all-cause mortality and cardiovascular mortality in MASLD patients.

The association between different insulin resistance surrogates and all-cause mortality and cardiovascular mortality in patients with metabolic dysfunction-associated steatotic liver disease.

Deubiquitinating enzymes (DUBs) are responsible for the removal of ubiquitin from substrates, thereby antagonizing ubiquitination and regulating a multitude of biological pathways including cell cycle progression, signal transduction, and transcriptional regulation. Ubiquitin Specific Protease-39 (USP39), a pivotal member of the ubiquitin-specific protease family, is intricately linked to innumerable pathophysiological processes. In this review, we first provide an overview of the specific structural domains and biological functions of USP39, with a particular focus on its role in DNA damage repair and RNA splicing processes. Then, we delineate the function of USP39 in maintaining epithelial morphology, resistance to viral infection, vascular remodeling, and pathological states. Moreover, we particularly focus on the aberrant expression of USP39 in various cancers and its effect on cancer markers, as well as on the regulatory role of USP39 in tumor progression. In conclusion, a comprehensive analysis of the structural domains and functional properties of USP39, a detailed investigation into its interaction mechanisms with diverse substrates, and the accelerated development of related inhibitors will provide a novel theoretical foundation for the treatment of numerous diseases, including tumors. Importantly, targeting USP39 may overcome resistance to checkpoint inhibitors, offering a promising approach to enhance cancer immunotherapy efficacy.

USP39 at the crossroads of cancer immunity: regulating immune evasion and immunotherapy response through RNA splicing and ubiquitin signaling.

Bladder cancer (BLCA) is one of the most invasive and malignant tumors in the world, thus leading to the urgent need of an accurate and recognizable biomarker. Several previous research has shown that Transient Receptor Potential Melastatin 4 (TRPM4) plays an important role in measuring vascular fragility and endothelial function. However, the role of TRPM4 in tumor hasn't been explored.

Article	Year
Comparative outcomes of radio frequency ablation versus partial nephrectomy for T1 renal tumors: a systematic review. Translational andrology and urology\| PubMed ID: 32038956	2019
Upregulation of KIF20A promotes tumor proliferation and invasion in renal clear cell carcinoma and is associated with adverse clinical outcome. Aging\| PubMed ID: 33232285	2020
Identification of novel autophagy-related lncRNAs associated with a poor prognosis of colon adenocarcinoma through bioinformatics analysis. Scientific reports\| PubMed ID: 33850225	2021
An integrated investigation of sulfotransferases (SULTs) in hepatocellular carcinoma and identification of the role of SULT2A1 on stemness. Apoptosis : an international journal on programmed cell death\| PubMed ID: 38411862	2024
A review: targeting UBR5 domains to mediate emerging roles and mechanisms - chance or necessity? International journal of surgery (London, England)\| PubMed ID: 38701508	2024
Emerging discoveries on the role of TRIM14: from diseases to immune regulation. Cell death discovery\| PubMed ID: 39719450	2024
The association between different insulin resistance surrogates and all-cause mortality and cardiovascular mortality in patients with metabolic dysfunction-associated steatotic liver disease... Cardiovascular diabetology\| PubMed ID: 40346671	2025
USP39 at the crossroads of cancer immunity: regulating immune evasion and immunotherapy response through RNA splicing and ubiquitin signaling. Frontiers in immunology\| PubMed ID: 40990019	2025
Transient Receptor Potential Melastatin 4 (TRPM4) is associated with an immuno-stimulatory TME and better prognosis in BLCA. Discover oncology\| PubMed ID: 41266683	2025

Yunxin Li

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