Multi-omics profiling highlights RPLP0 as a potential biomarker for prognosis and response to immunotherapy in clear cell renal cell carcinoma.

CARS1 as a Prognostic Biomarker and Candidate Therapeutic Vulnerability in Hepatocellular Carcinoma: Insights Into Tumor Progression and the Immune Microenvironment.

BACKGROUND Cysteinyl-tRNA synthetase 1 (CARS1) has been included in ferroptosis-related prognostic signatures, but its clinicopathological relevance, cellular functions, and relationship with the immune microenvironment in hepatocellular carcinoma (HCC) remain incompletely characterized. METHODS Transcriptomic and clinical data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset were integrated with corresponding data from an institutional HCC tissue cohort of 60 patients. CARS1 expression was evaluated by immunohistochemistry, and immune infiltration was examined using single-sample gene-set enrichment analysis (ssGSEA) and multiplex immunofluorescence, as well as by analyzing public single-cell datasets. The effects of CARS1 depletion were evaluated in MHCC97H and Hep3B cells using Cell Counting Kit-8 (CCK-8) assays, cell-cycle profiling, wound-healing assays, Transwell migration assays, western blotting, and erlotinib-sensitivity assays. RESULTS CARS1 expression was elevated in HCC and was associated with adverse clinicopathological features and poor overall survival. Quantitative immunohistochemistry confirmed elevated CARS1 protein expression in tumor tissues. CARS1 depletion inhibited cell proliferation, altered cell-cycle distribution, impaired migration, and enhanced in vitro sensitivity to erlotinib. High CARS1 expression was also associated with increased infiltration of Th2-like immune cells. CONCLUSIONS Elevated CARS1 expression is associated with an adverse biological and immune phenotype in HCC. These clinical, histopathological, and loss-of-function findings support further investigation of CARS1 as a prognostic marker and candidate therapeutic target in HCC, although additional mechanistic and in vivo validation is required.

Integrative omics profiling of CRELD2 in ccRCC: a nexus of genetics, prognosis, and tumor microenvironment

ARHGAP22 as a Potential Prognostic Biomarker in Clear Cell Renal Cell Carcinoma: Insights into Tumor Immunity and Co-Expression Networks.

Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer and is characterized by substantial clinical heterogeneity, highlighting the need for reliable prognostic biomarkers. This study evaluated the expression pattern, prognostic relevance, and immune-related associations of ARHGAP22 in ccRCC using transcriptomic and clinical data from The Cancer Genome Atlas Kidney Renal Clear Cell Carcinoma (TCGA-KIRC) cohort, together with external validation data and protein-expression information from the Human Protein Atlas (HPA). ARHGAP22 expression was compared between tumor and adjacent normal tissues, and its associations with overall survival, clinicopathological characteristics, tumor microenvironment scores, and estimated immune-cell fractions were assessed. Co-expression and functional-enrichment analyses were also performed to characterize potential biological associations. ARHGAP22 was significantly upregulated in ccRCC tissues at the transcriptomic level, with corresponding differences observed in immunohistochemical images. High ARHGAP22 expression was associated with shorter overall survival, advanced clinicopathological features, and higher ImmuneScore, StromalScore, and ESTIMATEScore values. CIBERSORT-based analysis showed that the high-expression group had higher estimated fractions of M2 macrophages and regulatory T cells and lower estimated fractions of naïve B cells, resting mast cells, and activated dendritic cells after false discovery rate correction. Functional-enrichment analyses linked ARHGAP22-associated genes to immune-related processes, cell migration, and chemokine- and cytokine-mediated signaling pathways. These findings suggest that ARHGAP22 may represent a potential prognostic and immune-related biomarker in ccRCC, although further independent clinical and experimental validation is required.

HKDC1 as a Prognostic and Tumor Microenvironment‑Associated Biomarker in Colorectal Cancer: An Integrated Multi‑omics and Spatial Transcriptomic Study.

LINC00460 drives clear cell renal cell carcinoma progression via complement/coagulation and p53 pathways: a potential therapeutic target.

This study demonstrates that the long noncoding RNA (lncRNA) LINC00460 is significantly overexpressed in clear cell renal cell carcinoma (ccRCC) and is strongly associated with adverse clinical outcomes. Analysis of data from The Cancer Genome Atlas (TCGA), validated by an independent cohort (GSE53757) and quantitative real-time polymerase chain reaction (qRT-PCR), shows that high LINC00460 expression has robust diagnostic value (area under the curve [AUC] = 0.818) and predicts shorter overall survival, highlighting its potential as a prognostic biomarker. Functional enrichment analyses indicate that LINC00460 is involved in key pathways, including complement and coagulation cascades, cytokine-cytokine receptor interactions, extracellular matrix remodeling, and p53 signaling. In vitro experiments confirm that silencing LINC00460 in ccRCC cell lines (Caki-2 and ACHN) markedly inhibits tumor cell proliferation, migration, and invasion while promoting apoptosis. Mechanistically, LINC00460 knockdown reduces levels of inflammatory factors (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-α], and C-X-C motif chemokine ligand 8 [CXCL8]) and coagulation-related proteins (C3, SERPINA1, and PLAU), and activates the p53 pathway by upregulating p21 and BAX while downregulating Bcl-2. Genomic analysis reveals higher mutation rates of BAP1 and LRP2 in LINC00460-high tumors, and drug repurposing screening identifies cinchonine and iproniazid as candidate therapeutic agents. These findings establish LINC00460 as an oncogenic driver in ccRCC and a promising target for both diagnosis and precision therapy.

Transcriptomic network analysis and functional evidence identify a candidate EMT hub signature associated with nasopharyngeal carcinoma progression.