Publications by authors named "Censhan Lin"
Article Synopsis
- Metastasis significantly contributes to the high mortality rate in lung cancer, yet the molecular mechanisms behind it remain unclear.
- Research revealed that diacylglycerol kinase alpha (DGKA) is overexpressed in metastatic non-small cell lung cancer (NSCLC) and is associated with poorer survival rates.
- DGKA interacts with SRC and FAK proteins, facilitating phosphorylation that triggers pathways linked to cancer progression, such as WNT/β-catenin and VEGF, which encourage processes like epithelial-mesenchymal transition (EMT) and angiogenesis, leading to metastasis.
- DGKA could serve as a valuable prognostic marker and a potential target for therapeutic interventions in NSCLC, particularly in cases with metastasis.
Metastasis is the leading cause of death of patients with esophageal squamous cell carcinoma (ESCC). Although an increasing number of studies have demonstrated the involvement of G3BP2 in several human cancers, how G3BP2 interacts with long noncoding RNAs and regulates mRNA transcripts in mediating ESCC metastasis remains unclear. In this study, we uncovered that G3BP2 was upregulated in ESCC.
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- The study investigates the role of nuclear pore complex protein Nup93 in hepatocellular carcinoma (HCC) progression and metastasis, analyzing data from 729 HCC cases.
- Elevated levels of Nup93 were found in HCC tissues, particularly in metastatic cases, and were associated with poorer patient prognosis.
- Nup93 was shown to enhance HCC cell growth and spread by regulating β-catenin movement, suggesting that targeting the Nup93-β-catenin pathway could provide new therapeutic options for HCC treatment.
Background & Aims: Little is known about Epstein-Barr virus (EBV)-associated intrahepatic cholangiocarcinoma (EBVaICC) because of its rarity. We aimed to comprehensively investigate the clinicopathology, tumor immune microenvironment (TIME) and genomic landscape of this entity in southern China.
Methods: We evaluated 303 intrahepatic cholangiocarcinomas (ICCs) using in situ hybridization for EBV.
Background: Liver is a major metabolic organ containing many metabolic enzymes. Disorders of liver-specific enzymes can cause liver dysfunction and tumorigenesis. Previous studies indicated that 4-Hydroxyphenylpyruvate dioxygenase (HPD) plays an essential role in catalyzing the tyrosinolytic metabolism of 4-hydroxyphenylpyruvate to homogeneous acids in liver tissues.
View Article and Find Full Text PDFHepatocellular carcinogenesis is attributed to the reprogramming of cellular metabolism as a consequence of the alteration in metabolite-related gene regulation. Identifying the mechanism of aberrant metabolism is of great potential to provide novel targets for the treatment of hepatocellular carcinoma (HCC). Here, we demonstrated that glycogen synthase 2 (GYS2) restricted tumor growth in hepatitis B virus-related HCC via a negative feedback loop with p53.
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