Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
BACKGROUND Serine hydroxymethyltransferase 2 (SHMT2) is a key enzyme in one-carbon cell metabolism, including in liver cancer. However, the associations between SHMT2 expression at the gene and protein level and prognosis in patients with hepatocellular carcinoma (HCC) remains unknown. This study aimed to investigate the expression levels of SHMT2 in tumor tissue samples from patients with HCC and clinical outcome and the effects of silencing the expression of the SHMT2 gene in HepG2 cells. MATERIAL AND METHODS Expression levels of SHMT2 were evaluated in 144 cases of HCC using immunohistochemistry and correlated with clinicopathological factors using the chi-squared (χ²) test. The prognostic significance of SHMT2 expression was analyzed by univariate analysis and multivariate analysis. Twenty pairs of HCC tissue and adjacent normal liver tissue were compared for SHMT2 expression levels using quantitative reverse transcription polymerase chain reaction (qRT-PCR). HepG2 cells underwent SHMT2 gene silencing and MTT and transwell assays investigated cell proliferation and migration. Western blot was used to detect the expression of markers of epithelial-mesenchymal transition (EMT). RESULTS Expression levels of SHMT2 in HCC tissues were significantly correlated with tumor grade and hepatitis B virus (HBV) infection, and increased expression was an independent negative prognostic factor in patients with HCC (P=0.003). Increased expression of the SHMT2 gene promoted the proliferation and migration of the HepG2 HCC cell line. CONCLUSIONS Increased expression of SHMT2 was a negative prognostic biomarker in patients with HCC. Expression of the SHMT2 gene promoted the proliferation and migration of HepG2 HCC cells.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6691751 | PMC |
| http://dx.doi.org/10.12659/MSM.915754 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Multi-Omics and Clinical Validation Identify Key Glycolysis- and Immune-Related Genes in Sepsis.
Int J Gen Med
September 2025
Department of Geriatrics, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, People's Republic of China.
Background: Sepsis is characterized by profound immune and metabolic perturbations, with glycolysis serving as a pivotal modulator of immune responses. However, the molecular mechanisms linking glycolytic reprogramming to immune dysfunction remain poorly defined.
Methods: Transcriptomic profiles of sepsis were obtained from the Gene Expression Omnibus.
A myotropic AAV vector combined with skeletal muscle -regulatory elements improve glycogen clearance in mouse models of Pompe disease.
Mol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
View Article and Find Full Text PDFPRMT1-Mediated PARP1 Methylation Drives Lung Metastasis and Chemoresistance via P65 Activation in Triple-Negative Breast Cancer.
Research (Wash D C)
September 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Triple-negative breast cancer (TNBC) is the most aggressive breast cancer subtype, characterized by a high propensity for metastasis, poor prognosis, and limited treatment options. Research has demonstrated a substantial correlation between the expression of protein arginine N-methyltransferase 1 (PRMT1) and enhanced proliferation, metastasis, and poor outcomes in TNBC. However, the specific role of PRMT1 in lung metastasis and chemoresistance remains unclear.
View Article and Find Full Text PDFHuman lung cancer neutrophils generate NETs with preserved anti-tumor cytotoxicity but impaired anti-migratory activity.
Front Immunol
September 2025
Institute of Pulmonary Medicine, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
Neutrophil extracellular traps (NETs) are DNA-protein structures released during a form of programmed neutrophil death known as NETosis. While NETs have been implicated in both tumor inhibition and promotion, their functional role in cancer remains ambiguous. In this study, we compared the NET-forming capacity and functional effects of NETs derived from lung cancer (LC) patients and healthy donors (H).
View Article and Find Full Text PDFIntegrative profiling of lung cancer biomarkers EGFR, ALK, KRAS, and PD-1 with emphasis on nanomaterials-assisted immunomodulation and targeted therapy.
Front Immunol
September 2025
Department of Thoracic Surgery, Shenzhen People's Hospital (The First Affiliated Hospital, Southern University of Science and Technology; The Second Clinical Medical College, Jinan University), Shenzhen, Guangdong, China.
Background: Lung cancer remains the leading cause of cancer-related mortality globally, primarily due to late-stage diagnosis, molecular heterogeneity, and therapy resistance. Key biomarkers such as EGFR, ALK, KRAS, and PD-1 have revolutionized precision oncology; however, comprehensive structural and clinical validation of these targets is crucial to enhance therapeutic efficacy.
Methods: Protein sequences for EGFR, ALK, KRAS, and PD-1 were retrieved from UniProt and modeled using SWISS-MODEL to generate high-confidence 3D structures.