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Background: BCCIP was originally identified as a BRCA2 interacting protein in humans and Ustilago maydis. It had low expression in some human cancer tissues. However, recent research indicated that many caretaker genes are also necessary for cell viability and their expression could contribute to tumor progression.Aim: To characterize whether BCCIP is a caretaker gene in esophageal squamous cell carcinoma (ESCC).Methods: Western blotting and immunohistochemistry were used to measure the expression of BCCIP β. In vitro studies were used to verify the effects of BCCIP β in Eca109 cells.Results: Expression of BCCIP β was notably higher in tumor tissues of ESCC and Eca 109 cells. Meanwhile, the immunohistochemistry stain revealed that BCCIP β was positively correlated with clinical pathologic variables such as tumor size and tumor grade, as well as Ki-67, and prompted poor prognosis. In vitro studies such as starvation and refeeding assay along with BCCIP β-shRNA transfection assay demonstrated that BCCIP β expression promoted proliferation of ESCC cells. In addition, BCCIP β downregulation by silencing RNA significantly decreased the rate of colony formation, alleviated cellular apoptosis and increased the chemosensitivity of cisplatin.Conclusions: This research first put forward that BCCIP β is an oncogene in human ESCC and contributes to the poor outcome of the deadly disease. [ABSTRACT FROM AUTHOR]

ANXA10 (annexin A10) is a member of the annexin family, and its biological effects are mediated primarily through the calcium-dependent phospholipid-binding and calcium ion binding. We examined the gene expressions of the L5 spinal cord after spinal nerve ligation (SNL)-induced neuropathic pain in mice by gene chip. The results showed that Anxa10 mRNA was the most upregulated gene in annexin family with 73.7-fold increase. Although previous studies have reported that several annexins are involved in nociceptive pain, the role of Anxa10 in pain remains undefined. We aimed to evaluate the role of ANXA10 in mediating injury-induced heat hyperalgesia and mechanical allodynia. We found that SNL induced persistent upregulation of Anxa10 mRNA and protein in the spinal cord of mice. Moreover, ANXA10 was colocalized with the neuronal marker MAP2 and astrocytic marker glial fibrillary acidic protein (GFAP), but not with microglial marker CD11b. Finally, pretreatment with Anxa10 siRNA partially prevented SNL-induced mechanical allodynia and heat hyperalgesia. Posttreatment with Anxa10 siRNA attenuated SNL-induced neuropathic pain. These findings suggest that ANXA10 might be a novel target in the treatment of neuropathic pain. [ABSTRACT FROM AUTHOR]

Abstract: Background: Caspase 3 associated with apoptosis and inflammation plays a key role in ischemia–reperfusion injury. The efficacy of naked caspase 3 small interfering RNA (siRNA) has been proved in an isolated porcine kidney perfusion model but not in autotransplantation. Materials and methods: The left kidney was retrieved from mini pigs and infused with the University of Wisconsin solution with or without 0.3mg of caspase 3 siRNA into the renal artery with the renal artery and vein clamped for 24-h cold storage (CS). After right nephrectomy, the left kidney was autotransplanted into the right for 48h without systemic treatment of siRNA. Results: Fluorescent dye–labeled caspase 3 siRNA was visualized in the post-CS kidneys but was weakened after transplantation. The expression of caspase 3 messenger RNA and precursor was downregulated by siRNA in the post-CS kidneys. In the siRNA-preserved posttransplant kidneys, however, the caspase 3 messenger RNA and active subunit were upregulated with further decreased precursor but increased active caspase 3+ cells, apoptotic cells, and myeloperoxidase+ cells. Moreover, the renal tissue damage was aggravated by siRNA, whereas the renal function was not significantly changed. Conclusions: Naked caspase 3 siRNA administered into the kidney was effective in cold preservation but not enough to protect posttransplant kidneys, which might be because of systemic complementary responses overcoming local effects. [Copyright &y& Elsevier]