Expression and clinical correlation of Survivin and PTEN in gastric cancer patients

Abstract

Reports on the correlation between the expression of Survivin/phosphatase and tensin homolog (PTEN) proteins and clinical factors in gastric cancer (GC) are varied, and the sample sizes were also not sufficient. The present study aimed to detect the expression of Survivin and PTEN proteins in GC patients on the basis of a greater number of specimens and to analyze the correlation with clinical features and survival. The results revealed that the Survivin expression rates in GC, normal tissues and metastatic lymph nodes were 72% (232/322), 5% (6/120) and 80% (36/45), respectively, while the PTEN expression rates were 34% (109/322), 92.5% (111/120) and 24.4% (11/45), respectively, and the differences between cancer and normal tissue or metastatic lymph nodes were significant for both proteins (P<0.05). The expression of Survivin was significantly associated with gross type, depth of invasion, distant metastasis, tumor, necrosis and metastasis (TNM) stage and vascular invasion, while PTEN expression was predominantly associated with age, tumor size, invasion depth, TNM stage and lymphatic invasion in GC patients (P<0.05). The expression of both was associated with postoperative metastasis and metastatic site (P= 0.007 and P= 0.011 for Survivin, and P= 0.002 and P= 0.005 for PTEN). There was a negative association between the expression levels of Survivin and PTEN (P= 0.001, r=-0.524). The expression levels of both were also associated with prognosis. The expression of Survivin and PTEN protein exhibit opposing trends in GC, which may indicate adverse biological effects in the occurrence of GC. The Survivin and PTEN expression levels are likely to be an important molecular event in gastric tumorigenesis and may be considered as molecular markers of GC progression and reliable prognostic indicators of GC.

Development of Multi-Scale X-ray Fluorescence Tomography for Examination of Nanocomposite-Treated Biological Samples

“…While we still must do IHC on exactly the same silicone nitride widows scanned by XFM in order to provide the final confirmation that nanocomposites colocalize with BIRC5, imaging of single cells analogous to work shown in Figure 4 may provide us with additional proofs for this possibility. BIRC5 plays numerous roles in carcinogenesis and metastasis, and has therefore been targeted by different small molecule, antibody, and nanocomposite therapies, both on its own or through its binding with Hsp90 [54,56,[62][63][64][65][66][67][68][69]. In this work, we found that non-targeted dopamine-coated Fe 3 O 4 @TiO 2 nanocomposites have a high affinity for BIRC5, making it one of the proteins of the "hard" protein corona.…”

Comprehensive biological information analysis of PTEN gene in pan-cancer

“…Our results showed that PTEN was down-regulated in all 17 different cancers studied, which is in agreement with earlier reports about PTEN showing decreased somatic expression of PTEN in various tumor types. In fact, low expression of PTEN has been reported in gastric cancer [29], prostate cancer [30], liver cancer [31], colorectal cancer [32], etc. This was also con rmed in our data.…”

Chemopreventive Effect of Metformin on Gastric Cancer Development

“…This cripples the IGF signaling pathway that facilitates the proliferation of cancer cells expressing IGF receptors. 22 Secondly, the activation of adenosine monophosphate-activated protein kinase (AMPK) and the subsequent inhibition of the mammalian target of rapamycin complex 1 pathway and survivin (one of the inhibitor of apoptosis proteins family that is associated with poor prognosis in GC) 66,67 is shown to induce cancer cell apoptosis. 68,69 Other potential direct anti-carcinogenic mechanisms of metformin include anti-proliferative effect on gastric cell lines causing G1 cell-cycle arrest, 70,71 the inhibition of the Wnt-β-catenin pathway, 72 a reversal of epithelial-to-mesenchymal transition, [73][74][75] AMPK-dependent inhibition of the sonic hedgehog signaling pathway, 76 which is essential for the maintenance of self-renewal and chemoresistance of cancer stem cells, and targeting cancer stem cells and progenitor cells.…”