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Suppressive expression of CD274 increases tumorigenesis and cancer stem cell phenotypes in cholangiocarcinoma

  1. Top of page
  2. Suppressive expression of CD274 increases tumorigenesis and cancer stem cell phenotypes in cholangiocarcinoma
  3. LIM protein JUB promotes epithelial–mesenchymal transition in colorectal cancer
  4. Stathmin1 regulates p27 expression, proliferation, and drug resistance, resulting in poor clinical prognosis in cholangiocarcinoma

Cholangiocarcinoma, cancer within the gall bladder, is the most common primary malignancy of the gastrointestinal tract. Despite its relatively high frequency, treatment is limited and prognosis often dismal. In an effort to better understand the pathogenesis of cholangiocarcinoma, Tamai and colleagues investigated the role of a known immunomodulatory ligand, CD274, in the progression of cholangiocarcinoma in immunodeficient mice xenografted with human cancer cells. What these researchers found was that mice that showed low expression of CD274 had more aggressive disease progression than mice with high expression of CD274, who had less aggressive strains. These results echo the authors' clinical suspicion that by classifying CD274 into high and low expression groups, a more accurate prognostic picture can be assessed for each patient. This important piece of work lays the groundwork for clinical correlation studies and perhaps a new way of understanding this devastating disease.doi: 10.1111/cas.12406

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Page 667–74

LIM protein JUB promotes epithelial–mesenchymal transition in colorectal cancer

  1. Top of page
  2. Suppressive expression of CD274 increases tumorigenesis and cancer stem cell phenotypes in cholangiocarcinoma
  3. LIM protein JUB promotes epithelial–mesenchymal transition in colorectal cancer
  4. Stathmin1 regulates p27 expression, proliferation, and drug resistance, resulting in poor clinical prognosis in cholangiocarcinoma

The pathway to invasive colorectal cancer is a well-delineated series of steps that lead to metastasis. One of these steps is epithelial–mesenchymal transition, in which cancer cells change their identity to become more aggressive, more rapidly producing cells. Despite being a fundamental step in cancer progression, each biologic step in EMT is not fully delineated. In this noteworthy study, Liang and colleagues studied a number of regulatory proteins in the LIM family to attempt to correlate their activity with EMT progression. They found that only one LIM protein, JUB, was positively correlated with EMT progression in colorectal cancer cell lines, and when expressed ectopically, promoted motility, invasiveness, and EMT. This novel finding could provide the framework for a potential therapeutic target in a common and deadly disease.doi: 10.1111/cas.12404

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Page 660–6

Stathmin1 regulates p27 expression, proliferation, and drug resistance, resulting in poor clinical prognosis in cholangiocarcinoma

  1. Top of page
  2. Suppressive expression of CD274 increases tumorigenesis and cancer stem cell phenotypes in cholangiocarcinoma
  3. LIM protein JUB promotes epithelial–mesenchymal transition in colorectal cancer
  4. Stathmin1 regulates p27 expression, proliferation, and drug resistance, resulting in poor clinical prognosis in cholangiocarcinoma

Bile duct cancers are classified as either intrahepatic or extrahepatic. Extrahepatic cholangiocarcinoma (EHCC) carries a particularly poor prognosis and treatments for this disease are limited. To better understand the pathogenesis of this deadly disease, Watanabe and coworkers studied the cytosolic protein stathmin1 (STMN1), which is associated with a treatment-resistant form of EHCC. In a large number of tissue samples the authors were able to show that high expression levels of STMN1 were associated with poorer survival. They went on to show with RNAi that inhibition of STMN1 function improved the effectiveness of a commonly used chemotherapeutic agent, paclitaxel. Furthermore, STMN1 was associated with p27, which is involved in cell migration. Together, these findings further elucidate the mechanisms leading to the aggressive nature of EHCC.doi: 10.1111/cas.12417

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Page 690–6