Two-dimensional differential in-gel electrophoresis for identification of gastric cancer-specific protein markers

Abstract

Abstract. Gastric cancer is the second most common fatal malignancy in the world. Proteomics studies of clinical tumor samples have led to the identification of specific protein markers of gastric cancer detection and better understanding the carcinogenesis of gastric cancer. Gastric cancer tissue of epithelial origin and adjacent normal mucosa were examined in pair by fluorescence 2-D differential in-gel electrophoresis proteomics analysis utilizing 2-D PAGE protein separation. Intensity changes of 33 spots were detected with statistical significance. Twenty-two out of the 33 spots were identified by MALDI-TOF MS or MS/MS. Of the 9 up-regulated proteins, 7 were identified, including heat shock protein 60 (HSP60), mutant desmin, effector cell proteinase receptor 1 splice form 1b, hypothetical protein, unnamed protein product, and manganese superoxide dismutase (MnSOD), a protein similar to ·-actin. Of the 20 down-regulated proteins, 16 were identified, including selenium binding protein 1, fibrinogen Á, HSP27, tubulin · 6, zinc finger protein 160, prostaglandin F synthase, and eukaryotic translation elongation factor 1 · 1. Our results suggest that MnSOD may be a potential serum marker for molecular diagnosis of gastric carcinoma, and DIGE is a useful technique for screening differentially expressed proteins in cancer tissues.

<p>TIM-3 Participates in the Invasion and Metastasis of Nasopharyngeal Carcinoma via SMAD7/SMAD2/SNAIL1 Axis-Mediated Epithelial-Mesenchymal Transition</p>

“…Previous research showed that MMP2 and MMP9 can hydrolyze the extracellular matrix and promote invasion of tumor cells. 39 Our results demonstrated that the expression of MMP2 was significantly enhanced in 6-10B and CNE-2 cells following the overexpression of TIM-3. The expression of MMP9 was obviously enhanced in 6-10B cells.…”

HVEM has a broader expression than PD-L1 and constitutes a negative prognostic marker and potential treatment target for melanoma

“…This HVEM signature is essentially a mixture of genes involved in melanoma proliferation (MITF, CAPN3, MLANA, GNPTAB, CPN1, SOX10, and GYPC 40,41 ) and of genes involved in invasive melanoma features (CITED1, 42 ACP5, 43 LZTS1, 44 GAB2, 45 SNX10, 46 and RXRG 26,36 ); among these, it is interesting to note that targeting RXR signaling may delay relapse in melanoma 47 and that the MXI1 hypoxia responsive 48 gene is a putative tumor suppressor gene involved in melanoma progression. 35 Among the remaining genes, GAS7, ALX1, and S100AI were reported in the Rambow melanoma signature, 41 but their respective role(s) in melanocyte lineage biology is unclear.…”