Asian Pac J Cancer Prev, 15 (11), 4539-4543 IntroductionThere is close relationship between neoplasia and inflammation. Many cancers arise from sites of chronic inflammation or irritation, and an oncogenic change always induces an inflammatory microenvironment to promote development of tumors. Inflammatory conditions in selected organs increase the risk of cancer, and in the tumor microenvironment smoldering inflammation contributes to proliferation and cancer progression. Natural bioactive compounds exhibit anti-inflammatory modulation (Pan et al., 2009;Gupta et al., 2011). The dietary flavonoid quercetin and resveratrol have nonsteroidal anti-inflammatory activity that may have applications for anti-inflammation treatment (Donnelly et al., 2004;Tuñón et al., 2009). Our other experiment indicates that the pro-inflammatory cytokine IP-10 in co-cultured human esophageal cancer 9706 cells can be inhibited by the polyphenol quercetin. Prevention of cancer has to be associated with prevention of inflammation, especially chronic inflammation.Flavonoid quercetin is one kind of yellowish powdered crystalline compound, (C15H10O7 in structure with five OH groups), widespread in vegetables, fruits and some
CD133 was recently reported to be a cancer stem cell and prognostic marker. Quercetin is considered as a potential chemopreventive agent due to its involvement in suppression of oxidative stress, proliferation and metastasis. In this study, the expression of CD133/CD44 in esophageal carcinomas and Eca109/9706 cells was explored. In immunoflurorescence the locations of CD133 + and multidrug resistance 1 (MDR 1) + in the same E-cancer cells were coincident, mainly in cytomembranes. In esophageal squamous cell carcinomas detected by double/single immunocytochemistry, small CD133 + cells were located in the basal layer of stratified squamous epithelium, determined as CSLC (cancer stem like cells); CD44 + surrounding the cells appeared in diffuse pattern, and the larger CD44 + (hi) cells were mainly located in the prickle cell layer of the epithelium, as progenitor cells. In E-cancer cells exposed to nanoliposomal quercetin (nLQ with cytomembrane permeability), down-regulation of NF-κBp65, histone deacetylase 1 (HDAC1) and cyclin D1 and up-regulation of caspase-3 were shown by immunoblotting, and attenuated HDAC1 with nuclear translocation and promoted E-cadherin expression were demonstrated by immunocytochemistry. In particular, enhanced E-cadherin expression reflected the reversed epithelial mesenchymal transition (EMT) capacity of nLQ, acting as cancer attenuator/preventive agent. nLQ acting as an HDAC inhibitor induced apoptotic cells detected by TUNEL assay mediated via HDAC-NF-κB signaling. Apoptotic effects of liposomal quercetin (LQ, with cytomembrane-philia) combined with CD133 antiserum were also detected by CD133 immunocytochemistry combined with TUNEL assay. The combination could induce greater apoptotic effects than nLQ induced alone, suggesting a novel anti-CSC treatment strategy.
Esophageal squamous cell carcinoma (ESCC) is the most common cancer in China, and multidrug resistance (MDR) remains one of the biggest problems in ESCC chemotherapy. In this study, we aimed to investigate the mechanism of Caveolin-1, an integral membrane protein, on regulating ESCC MDR. First, immunohistochemistry was used to check the protein expression of Caveolin-1, MDR-related protein of P-glycoprotein (P-gp), and multidrug resistance protein 1 (MRP1) in 84 pathologically characterized ESCC tissues, matched adjacent tumor, and adjacent normal-looking tissues. The results showed that Caveolin-1 expression level was elevated in ESCC tissues than that of matched adjacent tumor and adjacent normal-looking tissues (P < 0.05), and the expression of Caveolin-1 has close correlation with P-gp and MRP1 during tumor genesis of ESCC (P = 0.034, P = 0.009, respectively). Then, Caveolin-1 overexpression and knockdown were used to investigate its effect on expressions of P-gp and MRP1 in ESCC cell line Ec9706. The messenger RNA (mRNA) and protein expression levels of P-gp and MRP1 were checked by real-time quantitative reverse transcription-PCR (qRT-PCR) and Western blot (WB). The results showed that Caveolin-1 overexpression significantly promotes the mRNA and protein expression of MRP1 (P < 0.05), while almost has no effect on the mRNA and protein expression of P-gp (P > 0.05); Cavoelin-1 knockdown inhibits the mRNA and protein expressions of both P-gp and MRP1 (P < 0.05). The similar result was found in another ESCC cell line Eca109. So, it is concluded that Caveolin-1 affects ESCC MDR by regulating the expressions of P-gp and MRP1; therefore, it can be taken as a significant marker and target in tumor therapy.
The aim of this paper was to study the expression level and localization of DNA polymerase beta (polbeta) and the difference in those among the human esophageal cancer focus, cancer adjacent and corresponding normal esophageal tissues. These three kinds of tissues were collected from surgically resected tissues in 17 patients with esophageal carcinoma in Linzhou, China. Each of a total of 51 tissue pieces was divided into two aliquots: one aliquot for detection of polbeta expression by in situ hybridization and by immunohistochemistry; another for detection of polbeta expression by RNA dot blot and immunoblotting. In the tissue specimens detected by in situ hybridization and immunohistochemistry, the cancer focus tissue had much stronger polbeta expression signals localized in the scattered heteromorphologic cancer cells. The cancer adjacent tissue exhibited slightly stronger polbeta signals mainly localized in the epithelial proliferating cells and the corresponding normal tissue displayed weak polbeta signals basically located in the epithelial basal cells. The difference in expression level of polbeta among the three kinds of tissues detected by RNA dot blot and immunoblotting was similar to the above results. Further, the truncated POLB could be demonstrated in both cancer focus and cancer adjacent tissues, but could not be found in the corresponding normal tissue in immunoblotting. The results suggest that the overexpression of polbeta with truncated form may be a potential biomarker for early diagnosis of human esophageal carcinoma.
The differentiation and apoptosis of human esophageal cancer cell Eca-109 can be induced after 24- and 48-h treatment with 8-Br-cAMP, respectively. Upregulation of wt p53, iNOS and downregulation of c-myc may be associated with differentiation and apoptosis of Eca-109 cells. Furthermore, upregulation of FasL, p38 kinase and caspase-3 as well as downregulation of bcl-2, and Fas may be involved in the apoptosis of Eca-109 cells.
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