The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Timothy J. Yeatman - One of the best experts on this subject based on the ideXlab platform.
-
Role of Src expression and activation in human Cancer
Oncogene, 2000Co-Authors: Rosalyn B. Irby, Timothy J. YeatmanAbstract:Since the original identification of a transmissible agent responsible for the Development of tumors in chickens, now known to be a retrovirus encoding the v-src gene, significant progress has been made in defining the potential functions of its human homolog, SRC. The product of the human SRC gene, c-Src, is found to be over-expressed and highly activated in a wide variety of human Cancers. The relationship between Src activation and Cancer progression appears to be significant. Moreover, Src may have an influence on the Development of the metastatic phenotype. This review discusses the data supporting a role for c-Src as a critical component of the signal transduction pathways that control Cancer Cell Development and growth, and provides the rationale for targeting Src in drug discovery efforts.
Wang Jaw Yuan - One of the best experts on this subject based on the ideXlab platform.
-
ITOC2 – 003. Store-operated calcium signaling in EGF-mediated COX-2 inflammatory gene activation in Cancer Cells
European Journal of Cancer, 2015Co-Authors: Wang Jaw YuanAbstract:Cyclooxygenase-2 (COX-2) is one of the most important inflammatory genes involved in solid tumour metastasis. Epidermal growth factor receptor (EGFR) also plays a key role in Cancer Cell Development. We compared the expression levels of EGFR and COX-2 between tumour and normal tissues from 20 CRC patients and studied the molecular mechanism of EGFR-mediated COX-2 gene expression in Cancer Cells. Our results indicated that COX-2 expression was markedly increased after EGF stimulation. COX-2 promoter analysis indicated the involvement of cyclic AMP-responsive element (CRE) and nuclear factor of activated T Cells/nuclear factor interleukin-6 (NFAT/NF-IL6)-binding sites in EGF-mediated signaling pathways. Furthermore, EGF-mediated COX activation was prevented by 2 aminoethoxydiphenyl borate (2-APB), a store-operated Ca2+ channel inhibitor. In conclusion, store-operated Ca2+ entry is involved in the activation of transcription factors (CREB/NFAT) that are responsible for delivering EGF-mediated signals to evoke inflammatory cascades and is eventually related to CRC tumourigenesis.
Renza Vento - One of the best experts on this subject based on the ideXlab platform.
-
RB1 in Cancer: Different mechanisms of RB1 inactivation and alterations of pRb pathway in tumorigenesis
Journal of cellular physiology, 2013Co-Authors: Riccardo Di Fiore, Antonella D'anneo, Giovanni Tesoriere, Renza VentoAbstract:Loss of RB1 gene is considered either a causal or an accelerating event in retinoblastoma. A variety of mechanisms inactivates RB1 gene, including intragenic mutations, loss of expression by methylation and chromosomal deletions, with effects which are species-and Cell type-specific. RB1 deletion can even lead to aneuploidy thus greatly increasing Cancer risk. The RB1gene is part of a larger gene family that includes RBL1 and RBL2, each of the three encoding structurally related proteins indicated as pRb, p107, and p130, respectively. The great interest in these genes and proteins springs from their ability to slow down neoplastic growth. pRb can associate with various proteins by which it can regulate a great number of Cellular activities. In particular, its association with the E2F transcription factor family allows the control of the main pRb functions, while the loss of these interactions greatly enhances Cancer Development. As RB1 gene, also pRb can be functionally inactivated through disparate mechanisms which are often tissue specific and dependent on the scenario of the involved tumor suppressors and oncogenes. The critical role of the context is complicated by the different functions played by the RB proteins and the E2F family members. In this review, we want to emphasize the importance of the mechanisms of RB1/pRb inactivation in inducing Cancer Cell Development. The review is divided in three chapters describing in succession the mechanisms of RB1 inactivation in Cancer Cells, the alterations of pRb pathway in tumorigenesis and the RB protein and E2F family in Cancer.
Jun-ping Liu - One of the best experts on this subject based on the ideXlab platform.
-
Molecular interactions between telomerase and the tumor suppressor protein p53 in vitro.
Oncogene, 1999Co-Authors: Ying Cao, Michael C. Berndt, John W. Funder, Jun-ping LiuAbstract:The telomere DNA polymerase (telomerase) and the tumor suppressor protein p53 are frequently associated with human Cancers, and activation of telomerase and inactivation of p53 involved in Cancer Cell immortalization. In this report, we demonstrate a direct interaction of telomerase with p53 in the nuclear lysates of human breast Cancer Cells, and with recombinant human p53, by affinity chromatography and immunoprecipitation. On activity criteria, the interaction is between the carboxyl-terminal region of p53 and a region close to the amino-terminus of human telomerase-associated protein 1 (hTEP1). Incubation of recombinant p53 with nuclear telomerase extracts results in inhibition of telomerase activity, with the C-terminal region of p53 being essential for inhibition. This effect is not mediated by binding to telomerase substrate DNA, but requires the region near the N-terminus of hTEP1, in that a synthetic peptide derived from this region of hTEP1 similarly inhibits telomerase activity. Together, these in vitro interactions between telomerase and p53 suggest that the activity of telomerase may be regulated by p53, down-regulation of which in turn would favor up-regulation of telomerase activity in Cancer Cell Development.
Wei Chiao Chang - One of the best experts on this subject based on the ideXlab platform.
-
Involvement of store-operated calcium signaling in EGF-mediated COX-2 gene activation in Cancer Cells.
Cellular signalling, 2011Co-Authors: Jaw-yuan Wang, Ben Kuen Chen, Yu Shiuan Wang, Yao Ting Tsai, Wei Chiao Chen, Wen Chang Chang, Ming-feng Hou, Wei Chiao ChangAbstract:Growing evidence shows that chronic inflammation drives the progression of colorectal Cancer (CRC). Cyclooxygenase-2 (COX-2) is one of the most important inflammatory genes involved in solid tumor metastasis. Epidermal growth factor receptor (EGFR) also plays a key role in Cancer Cell Development. We compared the expression levels of EGFR and COX-2 between tumor and normal tissues from 20 CRC patients and studied the molecular mechanism of EGFR-mediated COX-2 gene expression in Cancer Cells. Our results indicated that COX-2 expression was markedly increased after EGF stimulation. COX-2 promoter analysis indicated the involvement of cyclic AMP-responsive element (CRE) and nuclear factor of activated T Cells/nuclear factor interleukin-6 (NFAT/NF-IL6)-binding sites in EGF-mediated signaling pathways. Furthermore, EGF-mediated COX-2 activation was prevented by 2-aminoethoxydiphenyl borate (2-APB), a store-operated Ca(2+) channel inhibitor. Transfection of siRNA against ORAI1 or STIM1, the key regulators of store-operated Ca(2+) channels, showed significant inhibitory effects on EGF-mediated COX-2 expression. In conclusion, store-operated Ca(2+) entry is involved in the activation of transcription factors (CREB/NFAT) that are responsible for delivering EGF-mediated signals to evoke inflammatory cascades and is eventually related to CRC tumorigenesis.
