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H1299 Cells (h1299 + cell)
Selected AbstractsBiocompatible, Luminescent Silver@Phenol Formaldehyde Resin Core/Shell Nanospheres: Large-Scale Synthesis and Application for In Vivo Bioimaging,ADVANCED FUNCTIONAL MATERIALS, Issue 6 2008Shi-Rui Guo Abstract Biocompatible and green luminescent monodisperse silver/phenol formaldehyde resin core/shell spheres with controllable sizes, in the range of 180 to 1000 nm, and interesting architectures (centric, eccentric, and coenocytic core/shell spheres) have been synthesized by a facile one-step hydrothermal approach. These spheres can be used as bioimaging labels for human lung cancer H1299 cells. The results demonstrate that the nanoparticles can be internalized into cells and exhibit no cytotoxic effects, showing that such novel biocompatible core/shell structures can potentially be used as in vivo bioimaging labels. This facile one-pot polymerization and encapsulation technique may provide a useful tool to synthesize other core/shell particles that have potential application in biotechnology. [source] MicroRNA-34a is an important component of PRIMA-1-induced apoptotic network in human lung cancer cellsINTERNATIONAL JOURNAL OF CANCER, Issue 2 2010Wenrui Duan Abstract Restoration of p53 function in tumor cells would be an attractive strategy for lung cancer therapy because p53 mutations are found in more than 50% of lung cancers. The small molecule PRIMA-1 has been shown to restore the tumor suppression function of p53 and to induce apoptosis in human tumor cells. The mechanism of apoptosis induced by PRIMA-1 remains unclear. We investigated the effects of PRIMA-1 in apoptosis with Western immunoblot analysis, TaqMan microRNA real-time PCR, cell viability analysis and flow cytometry using human lung cancer cell lines containing mutant (H211 and H1155), wild-type (A549) or null (H1299) p53. PRIMA-1 induced massive apoptosis in the H211 and H1155 cells, but was less toxic to the A549 and H1299 cells. Western immunoblot analysis showed cleavage of PARP in H211 and H1155 cells but not in A549 and H1299 cells following treatment with PRIMA-1. In addition, p53 protein was also phosphorylated in H211 and H1155 cells. TaqMan microRNA assay showed that the expression of microRNA-34a was increased in the H211 and H1155 cells posttreatment. Knockdown microRNA-34a decreased the rate of apoptosis caused by PRIMA-1. The above results suggest that microRNA-34a is one of the important components of PRIMA-1-induced apoptotic network in the cancer cells harboring mutant p53. [source] Expression of ,CP-4 inhibits cell cycle progression and suppresses tumorigenicity of lung cancer cellsINTERNATIONAL JOURNAL OF CANCER, Issue 7 2008Zafira Castaño Abstract The protein ,CP-4 (also known as hnRNP E4) is an RNA binding protein encoded by a gene at 3p21, one of the most common altered regions in lung cancer. It has been proposed that ,CP-4 may function as a lung tumor suppressor. Lack of ,CP-4 expression is frequent in highly proliferative lung tumors and correlates with ,CP-4 allele losses. The aim of this study was to evaluate the effect of ,CP-4 on the tumorigenic capacity of lung cancer cells. ,CP-4 expression was induced by transient transfection or stable infection with recombinant retroviruses. Induction of ,CP-4 expression caused cell cycle arrest in G2/M in 3 out of the 7 lung cancer cell lines studied, while no effect on apoptosis was observed. Anchorage-independent growth and invasion capacity of H1299 cells were significantly reduced by ,CP-4 induction. Tumorigenicity of H1299 cells in nude mice was greatly inhibited by the expression of ,CP-4. Moreover, induction of ,CP-4 expression in already established tumors resulted in a sudden growth arrest. Immunocytochemistry analysis of the xenograft tumors revealed an in vivo effect of ,CP-4 on cell proliferation and no effect on apoptosis. Finally, ,CP-4 showed a subcellular localization different from ,CP-4a, a splice variant that does not affect cell proliferation. In conclusion, expression of ,CP-4 can inhibit proliferation and tumorigenesis of lung cancer cells, both in vivo and in vitro, by delaying the progression of the cell cycle. © 2007 Wiley-Liss, Inc. [source] p53 cooperates berberine-induced growth inhibition and apoptosis of non-small cell human lung cancer cells in vitro and tumor xenograft growth in vivoMOLECULAR CARCINOGENESIS, Issue 1 2009Santosh K. Katiyar Abstract Berberine has been shown to have anti-carcinogenic effects. Since p53 is the most commonly mutated tumor suppressor gene, and a lack of functional p53 is associated with an increased risk of cancer development, we examined the effects of berberine on p53-positive and p53-deficient non-small cell human lung cancer cells in vitro and in vivo. Treatment of A549, which express wild-type p53, and H1299, which are p53-deficient, human lung cancer cells with berberine resulted in inhibition of cell proliferation and an increase in apoptotic cell death; however, A549 cells were more sensitive to the berberine-induced cytotoxic effects than H1299 cells. Further, the treatment of A549 cells with pifithrin-,, a specific inhibitor of p53, or transfection of A549 cells with a p53 antisense oligodeoxynucleotide resulted in a reduction in the berberine-induced inhibition of cell proliferation and apoptosis. The berberine-induced apoptosis of both the A549 and H1299 human lung cancer cells was associated with the disruption of mitochondrial membrane potential, reduction in the levels of Bcl-2, Bcl-xl while increase in Bax, Bak, and activation of caspase-3. Treatment of the cells with pan-caspase inhibitor (z-VAD-fmk) or caspase-3 inhibitor (z-DEVD-fmk) inhibited berberine-induced apoptosis, thus suggesting the role of caspase-3. Further, the administration of berberine by oral gavage inhibited the growth of s.c. A549 and H1299 lung tumor xenografts in athymic nude mice, however, the growth of tumor xenograft of H1299 cells was faster than A549 cells in mice and the chemotherapeutic effect of berberine was more pronounced in the p53-positive-A549 tumor xenograft than p53-deficient-H1299 tumor xenograft. © 2008 Wiley-Liss, Inc. [source] Monodemethylated polymethoxyflavones from sweet orange (Citrus sinensis) peel Inhibit growth of human lung cancer cells by apoptosisMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 3 2009Hang Xiao Abstract Polymethoxyflavones (PMFs) are almost exclusively found in the Citrus genus, particularly in the peels of sweet orange (Citrus sinensis L. Osbeck) and mandarin (C. reticulate Blanco). We studied the effects of two major PMFs, namely, nobiletin and 3,5,6,7,8,3,,4,-heptamethoxyflavone (HMF), and two major monodemethylated PMFs, namely 5-hydroxy-3,7,8,3,,4,-pentamethoxyflavone (5HPMF), and 5-hydroxy-3,6,7,8,3,,4,-hexamethoxyflavone (5HHMF), on the growth of human lung cancer H1299, H441, and H460 cells. Monodemethylated PMFs were much more potent in growth inhibition of lung cancer cells than their permethoxylated counterpart PMFs. In H1299 cells, cell cycle analyses further revealed that monodemethylated PMFs caused significant increase in sub-G0/G1 phase, suggesting possible role of apoptosis in the growth inhibition observed, whereas the permethoxylated counterpart PMFs did not affect cell cycle distribution at same concentrations tested. These results strongly suggested that the phenolic group is essential for the growth inhibitory activity of monodemethylated PMFs. Further studies in H1299 cells demonstrated that monodemethylated PMFs downregulated oncogenic proteins, such as iNOS, COX-2, Mcl-1, and K-ras, as well as induced apoptosis evidenced by activation of caspase-3 and cleavage of PARP. Our results provide rationale to develop orange peel extract enriched with monodemethylated PMFs into value-added nutraceutical products for cancer prevention. [source] | ||||||||||