39
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Chinese herb related molecules of cancer-cell-apoptosis: a minireview of progress between Kanglaite injection and related genes

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Many kinds of Chinese herb had been confirmed to have the character of anti-tumor, clinical reports about anti-tumor effects of Chinese herb had also been found in recent years, but most of the reports were focused on the clinical treatment of effectiveness for Chinese herb, on the other hand, review about Chinese herbal related with molecules on cancer-cell-apoptosis was seldom, many scientists could not believe such kinds of clinical describes about anti-tumor effects for Chinese herb, because these describes were lack of molecular biology evidence. Kanglaite(KLT) injection is an anti-tumor new drug which extracts from Chinese medicine- coix seed with modern advanced pharmaceutical technology, it is also a new biphase extended-spectrum anticancer medicine, the food and drug administration(FDA) of United States also approved a phase II trial of KLT to test its efficacy in treating non-small-cell lung cancer. Some studies show it could inhibit some anti-apoptotic gene and activate some pro-apoptotic gene, its injection solution is one of the new anticancer medicine that can significantly inhibit a various kinds of tumor cells, so it has become the core of research that how to further explore KLT injection to promote tumor cell apoptosis by impacting on related genes. In this review, the relationship between KLT and some tumor cell apoptosis molecules had been discussed and reviewed generally.

          Related collections

          Most cited references58

          • Record: found
          • Abstract: found
          • Article: not found

          Solution structure of BID, an intracellular amplifier of apoptotic signaling.

          We report the solution structure of BID, an intracellular cross-talk agent that can amplify FAS/TNF apoptotic signal through the mitochondria death pathway after Caspase 8 cleavage. BID contains eight alpha helices where two central hydrophobic helices are surrounded by six amphipathic ones. The fold resembles poreforming bacterial toxins and shows similarity to BCL-XL although sequence homology to BCL-XL is limited to the 16-residue BH3 domain. Furthermore, we modeled a complex of BCL-XL and BID by aligning the BID and BAK BH3 motifs in the known BCL-XL-BAK BH3 complex. Additionally, we show that the overall structure of BID is preserved after cleavage by Caspase 8. We propose that BID has both BH3 domain-dependent and -independent modes of action in inducing mitochondrial damage.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The role of c-myc in cellular growth control.

            E. Schmidt (1999)
            Cell division is coupled to cell growth. Since some c-myc target genes are regulators of cell growth while others function in cell division pathways, c-myc is apparently poised at the interface of these processes. Cell culture systems have shown specific myc-associated growth phenotypes. Increased cell growth precedes DNA synthesis after myc activation in cells expressing myc-estrogen receptor fuson constructs and cells lacking c-myc exhibit a marked loss of protein synthesis. A number of candidate c-myc target genes regulate processes required for cell growth including rRNA transcription and processing, ribosomal protein transcription and translation, and translation initiation. These interactions all have the potential to account for the growth phenotypes in c-myc mutant cells. The ability of translation initiation factors, including eIF4E, to transform cells makes them particularly interesting targets of c-myc. Further evaluation of these target genes will provide important insights into growth control and c-myc's functions in cellular proliferation.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              The transcriptional coactivator and acetyltransferase p300 in fibroblast biology and fibrosis.

              The transcriptional coactivator p300 is a ubiquitous nuclear phosphoprotein and transcriptional cofactor with intrinsic acetyltransferase activity. p300 controls the expression of numerous genes in cell-type and signal-specific manner, and plays a pivotal role in cellular proliferation, apoptosis, and embryogenesis. By catalyzing acetylation of histones and transcription factors, p300 plays a significant role in epigenetic regulation. Recent evidence suggests that abnormal p300 function is associated with deregulated target gene expression, and is implicated in inflammation, cancer, cardiac hypertrophy, and genetic disorders such as the Rubinstein-Taybi syndrome. The activity of p300 is regulated at multiple levels, including developmental stage-specific expression, post-translational modifications, subcellular localization, and cell-type and gene-specific interactions with transcription factors. Although p300 has been investigated extensively in epithelial and hematopoietic cells, its role in fibroblast biology and tissue repair has received little attention to date. Recent studies implicate p300 in the regulation of collagen synthesis by transforming growth factor-beta (TGF-beta). Both the acetyltransferase activity of p300 and its inducible interaction with Smad3 are essential for mediating TGF-beta-induced stimulation of collagen synthesis. As a signal integrator whose availability for intracellular interactions with transcription factors is strictly limiting, p300 mediates the antagonistic regulation of TGF-beta-induced collagen synthesis by IFN-gamma and TNF-alpha via intracellular competition for limiting amount of p300. Significantly, p300 is itself a direct transcriptional target of TGF-beta in normal fibroblasts, and its levels are significantly elevated in fibrotic lesions as well as in experimental models of fibrosis. The emerging appreciation of the importance of p300 in extracellular matrix (ECM) remodeling and fibrosis and novel insights concerning the regulation, mechanism of action, and significance of p300 in fibroblast biology are discussed in this minireview. 2007 Wiley-Liss, Inc.
                Bookmark

                Author and article information

                Journal
                J Exp Clin Cancer Res
                Journal of Experimental & Clinical Cancer Research : CR
                BioMed Central
                0392-9078
                1756-9966
                2008
                21 August 2008
                : 27
                : 1
                : 31
                Affiliations
                [1 ]Department of Hepatobiliary Surgery, Affiliated Hospital of Medical College, Qingdao University, No.16 Jiangsu Rd, Qingdao 266003, PR China
                [2 ]Center of Cell and Molecular Pathology, Affiliated Hospital of Medical College, Qingdao University, No.16 Jiangsu Rd, Qingdao 266003, PR China
                [3 ]Department of Pediatric Surgery, Affiliated Hospital of Medical College, Qingdao University, No.16 Jiangsu Rd, Qingdao 266003, PR China
                Article
                1756-9966-27-31
                10.1186/1756-9966-27-31
                2543009
                18718024
                e35a5e02-404e-44a5-86c4-65499944ca4e
                Copyright © 2008 Lu et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 June 2008
                : 21 August 2008
                Categories
                Review

                Oncology & Radiotherapy
                Oncology & Radiotherapy

                Comments

                Comment on this article