• 2019-10
  • 2019-11
  • 2020-03
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  • 13826-64-7 br In addition to directly eliminating CD CSCs an


    In addition to directly eliminating CD133+ CSCs, another alter-native is to decrease CD133 expression in CSCs through modulation of the signaling molecules that regulate CD133 transcription and expres-sion. Other feasible targets are the CD133 downstream signaling mo-lecules that mediate metastasis and multi-drug resistance. Of note, in-direct targeting CD133 via the cell signaling molecules can be highly specific to cancer types due to the unique cell environment in each type of cancer.
    6. Summary
    Tumor metastasis and therapeutic resistance account for the ma-jority of cancer-related deaths. Both properties are enhanced in a small population of CD133high cancer cells, known as cancer stem 13826-64-7 with r> abilities of self-renewal, tumor initiation, and pluripotency. Therefore, targeting cancer stem cells, such as CD133high cell populations remains one of top interest to combat fatalities of cancer patients. Elevated expression of CD133 resulted in increased tumor-initiating ability, tumor progression, metastasis, therapeutic resistance, and cancer re-currence in numerous types of cancer. Targeting CSC population so far remains certain challenges because of its heterogeneity. It would be of most importance to evaluate if the blockade of CD133 alternatively results in selections for other cancer stem cell markers that could compensate the loss of CD133, and what the final outcome of cancer metastasis as well as drug resistance is in animal models capitulating human cancers.
    Competing interests
    The author declares no competing interests on publication of this article.
    Ethics approval and consent to participate
    All animal experiments were approved by the Atlanta University Center IACUC committee (protocol #: 17-20) and performed in ac-cordance with relevant institutional and national guidelines and reg-ulations.
    Ding, Q., Miyazaki, Y., Tsukasa, K., Matsubara, S., Yoshimitsu, M., Takao, S., 2014. CD133 facilitates epithelial-mesenchymal transition through interaction with the ERK pathway in pancreatic cancer metastasis. Mol. Cancer 13, 15.
    Katoh, M., 2017. Canonical and non-canonical WNT signaling in cancer stem cells and their niches: cellular heterogeneity, omics reprogramming, targeted therapy and tumor plasticity (Review). Int. J. Oncol. 51, 1357–1369.
    Bardeesy, N., Storz, P., 2017. The presence of Interleukin-13 at pancreatic ADM/ PanIN lesions alters macrophage populations and mediates pancreatic tumorigenesis. Cell Rep. 19, 1322–1333.
    metastasis and vascular endothelial growth factor-C expression in pancreatic cancer.
    Permanyer, J., Navarro, R., Friedman, J., Pomares, E., Castro-Navarro, J., Marfany, G., Swaroop, A., Gonzalez-Duarte, R., 2010. Autosomal recessive retinitis pigmentosa with early macular affectation caused by premature truncation in PROM1. Invest. Ophthalmol. Vis. Sci. 51, 2656–2663.
    Tang, Y., Berlind, J., Mavila, N., 2018. Inhibition of CREB binding protein-beta-catenin signaling down regulates CD133 expression and activates PP2A-PTEN signaling in tumor initiating liver cancer cells. Cell Commun. Signal 16, 9.
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    CD155 expression and its prognostic value in postoperative patients with breast cancer 
    Hongmei Yonga,1, Ronghui Chenga,1, Xia Lib, Guangyi Gaoa, Xuan Jianga, Hongyun Chenga, Xueyi Zhoua, , Wei Zhaoc, a Department of Oncology, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huaian 223002, China b Department of Geriatrics, The Affiliated Huai’an Hospital of Xuzhou Medical University and The Second People’s Hospital of Huai’an, Huaian 223002, China c Department of Pathology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210021, China
    Breast cancer
    1. Introduction
    In China, the incidence rate of breast cancer (BC) is the highest among malignant tumors of the female reproductive system, and the mortality rate of BC is the fifth highest [1]. Surgery, chemotherapy, and radiotherapy are the three traditional treatments for breast cancer. Since the introduction of herceptin, the overall response (RR) and overall survival (OS) of patients with recurrent and advanced HER-2 positive BC have dramatically improved. However, the proportion of HER2 positive overexpressing breast cancer is only about 15–20% [2]. The treatment of the majority of BC patients lacking the HER-2 bio-marker still relies on surgery, chemotherapy and radiotherapy. The RR and OS of those treatments are relatively 13826-64-7 lower [3,4]. Therefore, it is necessary to search for new therapeutic targets in BC.