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Functional role of interaction between tumor necrosis factor-related apoptosis-inducing ligand and DR5 in B16F10 cells by activating the nuclear factor-κB pathway to induce metastatic potential

  1. Top of page
  2. Functional role of interaction between tumor necrosis factor-related apoptosis-inducing ligand and DR5 in B16F10 cells by activating the nuclear factor-κB pathway to induce metastatic potential
  3. Sorting nexin 2-mediated membrane trafficking of c-Met contributes to sensitivity of molecular targets
  4. Claudin-7 increases chemosensitivity to cisplatin through upregulation of caspase pathway in human NCI-H522 lung cancer cells
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Page 558–62

This study sheds light on one of the monumental obstacles to the use of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as a cancer treatment. Takahasi et al. show that, in a mouse model of malignant melanoma known to be insensitive to the apoptotic effects of TRAIL, TRAIL actually induced metastasis. It did this by working through the DR5 receptor to activate the nuclear factor-κB pathway, resulting not only in the appearance of factors that promote metastasis, such as MMP-9 and rapid cell proliferation, but also by actually inducing metastatic spread to the lung.

Sorting nexin 2-mediated membrane trafficking of c-Met contributes to sensitivity of molecular targets

  1. Top of page
  2. Functional role of interaction between tumor necrosis factor-related apoptosis-inducing ligand and DR5 in B16F10 cells by activating the nuclear factor-κB pathway to induce metastatic potential
  3. Sorting nexin 2-mediated membrane trafficking of c-Met contributes to sensitivity of molecular targets
  4. Claudin-7 increases chemosensitivity to cisplatin through upregulation of caspase pathway in human NCI-H522 lung cancer cells
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Page 573–83

Intracellular signaling plays a key role in the development and progression of cancer. The signaling cascades involved in cell growth, for example, rely on receptors and proteins within the cellular membrane and cytoplasm. Targeted therapies have been developed to inhibit the activity of epidermal growth factor receptor (EGFR) and are effective at slowing the growth of tumor cells, such as in lung cancer. However, cancers may become resistant to EGFR blockade through mechanisms such as c-Met protein overexpression. Ogi et al. hypothesized that reducing c-Met activity should improve responses to EGFR-targeted therapies. To test their hypothesis, the authors used siRNA to inhibit a protein that is critical to c-Met protein trafficking. By reducing the availability of c-Met in signal transduction, the researchers were able to boost the effects of EGFR-targeted anticancer therapies. These findings provide a new therapeutic strategy that could impact the treatment of EGFR-positive malignancies.

Claudin-7 increases chemosensitivity to cisplatin through upregulation of caspase pathway in human NCI-H522 lung cancer cells

  1. Top of page
  2. Functional role of interaction between tumor necrosis factor-related apoptosis-inducing ligand and DR5 in B16F10 cells by activating the nuclear factor-κB pathway to induce metastatic potential
  3. Sorting nexin 2-mediated membrane trafficking of c-Met contributes to sensitivity of molecular targets
  4. Claudin-7 increases chemosensitivity to cisplatin through upregulation of caspase pathway in human NCI-H522 lung cancer cells
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Page 611–18

Small-cell carcinoma of the lung (SCCL) has a grave prognosis; it is known to quickly metastasize and many patients present with late-stage disease. Tight junctions are important in maintaining cell integrity and reducing the invasive potential of cells. They are also responsible for maintaining cell polarity, adhesion, and paracellular permeability. The lack of expression of a component of tight junctions, claudin 7, might contribute to the rapid spread of SCCL. Here, Hoggard et al. transfected human SCCL cells with claudin-7 then treated the cells with cisplastin, a standard chemotherapeutic agent in the treatment of SCCL. Results showed that cells that were transfected with claudin-7 had a significantly higher apoptotic rate than those SCCL cells that were not transfected. Furthermore, the researchers deduced that this rise in apoptosis was taking place through activation of the caspase pathway. Further understanding of this pathway could prove fruitful in the treatment of devastating cancers such as SCC of the lung.