Which organelle is responsible for protein synthesis

The increase of outer mitochondrial membrane permeability is a central event in apoptotic cell death, since it releases several apoptogenic factors such as cytochrome c into the cytoplasm that activate the downstream destructive processes. The voltage-dependent anion channel (VDAC or mitochondrial porin) plays an essential role in the increase of mitochondrial membrane permeability, and it is regulated by the Bcl-2 family of proteins via direct interaction.

Specialized Cell Structure and Function: Protein Synthesis

Most of the components of photosynthesis are located in the thylakoids.

The ribosome is the site of protein synthesis ..

We have recently shown in culture that cannabidiol was an effective inhibitor of Id-1 expression and corresponding breast cancer cell aggressiveness, that is, invasion and proliferation (25, 26). To determine whether cannabidiol could inhibit Id-1 expression in aggressive brain cancers, U251 cells were treated with cannabidiol for 3 days and analyzed for Id-1 protein using Western blot analysis. In U251 cells, cannabidiol produced a concentration-dependent downregulation of Id-1 (Fig. 6A). In addition, the downregulation of Id-1 expression correlated with a concentration-dependent inhibition of U251 cell invasion (Fig. 6B). Similar activity was observed in primary glioblastoma cells that express Id-1 (Fig. 6C and D). Moreover, cannabidiol modulated the phosphorylation of several phospho-kinases in U251 cells, including AKT

In the next phase of protein synthesis, ..

Mol Cancer Ther. 2007 Nov;6(11):2921-7.
Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.
McAllister SD1, Christian RT, Horowitz MP, Garcia A, Desprez PY.
Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 expression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.

Interactive Eukaryotic Cell Model - CELLS alive!

We predicted that CBD, the most potent inhibitor of breast cancer cell proliferation and invasion tested, would regulate the expression of key genes that control breast cancer cell proliferation and invasiveness. A potential candidate protein that could mediate the effects of CBD on both phenotypes was the helix-loop-helix protein Id-1. We determined that treatment of MDA-MB231 cells with CBD led to a concentration-dependent inhibition of Id-1 protein expression (Fig. 1B and C). The inhibitory effect of CBD on Id-1 expression occurred at concentrations as low as 100 nmol/L. CBD was significantly more effective at reducing Id-1 protein expression compared with other cannabinoid compounds (Fig. 1C). The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of MDA-MB231 cells. Furthermore, the down-regulation of Id-1 protein in the presence of CBD seemed to precede, and not follow, the inhibitory effects of CBD on the proliferation and invasiveness of MDA-MB231 cells (Fig. 1D), suggesting that Id-1 down-regulation represents a cause rather than a consequence of a decrease in breast cancer cell aggressiveness.

Protein Synthesis -Translation and Regulation

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J Cell Sci. 2000 Nov;113 ( Pt 22):3897-905.
ID helix-loop-helix proteins in cell growth, differentiation and tumorigenesis. Norton JD.
The ubiquitously expressed family of ID helix-loop-helix (HLH) proteins function as dominant negative regulators of basic HLH (bHLH) transcriptional regulators that drive cell lineage commitment and differentiation in metazoa. Recent data from cell line and in vivo studies have implicated the functions of ID proteins in other cellular processes besides negative regulation of cell differentiation. ID proteins play key roles in the regulation of lineage commitment, cell fate decisions and in the timing of differentiation during neurogenesis, lymphopoiesis and neovascularisation (angiogenesis). They are essential for embryogenesis and for cell cycle progression, and they function as positive regulators of cell proliferation. ID proteins also possess pro-apoptotic properties in a variety of cell types and function as cooperating or dominant oncoproteins in immortalisation of rodent and human cells and in tumour induction in Id-transgenic mice. In several human tumour types, the expression of ID proteins is deregulated, and loss- and gain-of-function studies implicate ID functions in the regulation of tumour growth, vascularisation, invasiveness and metastasis. More recent biochemical studies have also revealed an emerging ‘molecular promiscuity’ of mammalian ID proteins: they directly interact with and modulate the activities of several other families of transcriptional regulator, besides bHLH proteins.

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Id-1 (Inhibitor of differentiation/DNA binding) is a member of the helix-loop-helix protein family expressed in actively proliferating cells. It regulates gene transcription by heterodimerization with the basic helix-loop-helix transcription factors and therefore inhibits them from DNA binding and transactivation of their target genes. Early studies showed that Id-1 functions mainly as a regulator in cellular differentiation of the muscle cells. The oncogenic role of Id-1 was revealed recently by the finding that Id-1 expression was able to induce cancer cell growth and promote cell survival. In addition, Id-1 protein was frequently overexpressed in over 20 types of cancer, supporting its role in the tumorigenesis of a wide range of tissues. However, the fact that Id-1 was able to activate multiple pathways involved in tumor progression suggests that Id-1 may in addition function in promotion of tumor development. For example, overexpression of Id-1 was found to induce expression of MT1-MMP protein, leading to invasion of breast cancer cells. A close association between Id-1 expression and angiogenesis has also been demonstrated recently in both normal and cancer cells. Accordingly, in prostate cancer cells, expression of Id-1 was able to activate EGF-R and nuclear factor-kappaB activities and resulted in progression to androgen independence. In addition, in both nasopharyngeal carcinoma and prostate cancer cells, Id-1 expression was found to protect the cells from chemotherapeutic drug-induced apoptosis through regulation of the Raf-1/MAPK and JNK pathways. This review will discuss recent evidence supporting the role of Id-1 in tumor progression and the mechanisms involved.