40
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Overexpression of Class III β-tubulin, Sox2, and nuclear Survivin is predictive of taxane resistance in patients with stage III ovarian epithelial cancer.

      Read this article at

          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

          Class III β-tubulin, Sox2, and Survivin play important roles in tumor survival and proliferation. However, the association of these three factors with clinicopathological characteristics, chemoresistance, and survival in patients with ovarian cancer remains controversial.

          Related collections

          Most cited references39

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

          IAP family proteins--suppressors of apoptosis.

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

            A novel anti-apoptosis gene, survivin, expressed in cancer and lymphoma.

            Inhibitors of programmed cell death (apoptosis) aberrantly prolonging cell viability may contribute to cancer by facilitating the insurgence of mutations and by promoting resistance to therapy. Despite the identification of several new apoptosis inhibitors related to bcl-2 or to the baculovirus IAP gene, it is not clear whether apoptosis inhibition plays a general role in neoplasia. Here, we describe a new human gene encoding a structurally unique IAP apoptosis inhibitor, designated survivin. Survivin contains a single baculovirus IAP repeat and lacks a carboxyl-terminal RING finger. Present during fetal development, survivin is undetectable in terminally differentiated adult tissues. However, survivin becomes prominently expressed in transformed cell lines and in all the most common human cancers of lung, colon, pancreas, prostate and breast, in vivo. Survivin is also found in approximately 50% of high-grade non-Hodgkin's lymphomas (centroblastic, immunoblastic), but not in low-grade lymphomas (lymphocytic). Recombinant expression of survivin counteracts apoptosis of B lymphocyte precursors deprived of interleukin 3 (IL-3). These findings suggest that apoptosis inhibition may be a general feature of neoplasia and identify survivin as a potential new target for apoptosis-based therapy in cancer and lymphoma.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Tubulin-targeting chemotherapy impairs androgen receptor activity in prostate cancer.

              Recent insights into the regulation of the androgen receptor (AR) activity led to novel therapeutic targeting of AR function in prostate cancer patients. Docetaxel is an approved chemotherapy for treatment of castration-resistant prostate cancer; however, the mechanism underlying the action of this tubulin-targeting drug is not fully understood. This study investigates the contribution of microtubules and the cytoskeleton to androgen-mediated signaling and the consequences of their inhibition on AR activity in human prostate cancer. Tissue microarrays from docetaxel-treated and untreated prostate cancer patients were comparatively analyzed for prostate-specific antigen (PSA) and AR immunoreactivity. The AR transcriptional activity was determined in prostate cancer cells in vitro, based on PSA mRNA expression and the androgen response element reporter activity. The interaction of AR with tubulin was examined by immunoprecipitation and immunofluorescence. Treatment of prostate cancer patients with docetaxel led to a significant translocation of AR. In untreated specimens, 50% prostate tumor cells exhibited nuclear accumulation of AR, compared with docetaxel-treated tumors that had significantly depleted nuclear AR (38%), paralleled by an increase in cytosolic AR. AR nuclear localization correlated with PSA expression. In vitro, exposure of prostate cancer cells to paclitaxel (1 μmol/L) or nocodazole (5 μg/mL) inhibited androgen-dependent AR nuclear translocation by targeting AR association with tubulin. Introduction of a truncated AR indicated the requirement of the NH(2)-terminal domain for AR-tubulin interaction. Our findings show that in addition to blocking cell division, docetaxel impairs AR signaling, evidence that enables new insights into the therapeutic efficacy of microtubule-targeting drugs in prostate cancer. ©2010 AACR.
                Bookmark

                Author and article information

                Journal
                BMC Cancer
                BMC cancer
                Springer Science and Business Media LLC
                1471-2407
                1471-2407
                Jul 23 2015
                : 15
                Affiliations
                [1 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. jintongdu@sina.cn.
                [2 ] Shandong Cancer Hospital, Shandong Academy of Medical Science, Ji'nan, Shandong, 250012, China. jintongdu@sina.cn.
                [3 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. beili008@hotmail.com.
                [4 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. fyl1599@126.com.
                [5 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. y.g.liu@163.com.
                [6 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. 530623106@qq.com.
                [7 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. lijisheng@gmail.com.
                [8 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. wenzhou25@sdu.edu.cn.
                [9 ] Department of Chemotherapy, Qilu Hospital of Shandong University, No. 107 Wenhuaxi road, Ji'nan, Shandong, 250012, China. xiuwenwang12@sdu.edu.cn.
                Article
                10.1186/s12885-015-1553-x
                10.1186/s12885-015-1553-x
                4511538
                26198101
                ddb61035-23d9-4651-910b-28d6464f80bb
                History

                Comments

                Comment on this article