rdf-syntax-grammar
mods:
  schema location: http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
  title info:
    title: Molecular Mechanisms of Cannabinoids as Anti-cancer Agents
  name:
    name part: Sreevalsan, Sandeep
    role:
      role term: creator
    role:
      role term: author.
  name:
    name part: Safe, S.
    role:
      role term: thesis advisor.
  name:
    name part: Texas A & M University
    role:
      role term: degree granting institution.
  type of resource: text
  genre: bibliography
  origin info:
    place:
      place term: txu
    date issued: 2013
    issuance: monographic
  language:
    language term: eng
  physical description:
    form: remote
    extent: 1 online resource.
  abstract: Cancer is a growing health concern world-wide and is the second most common cause of death after heart diseases. Current treatment strategies such as surgery, chemotherapy and radiation provide some relief to cancer patients but the toxic side effects associated with chemotherapy and radiation often lead to further adverse health effects. Hence there is a need for drugs with better safety profile and improved efficacy. Cannabinoids are a group of compounds with several therapeutic properties and besides their appetite stimulant, anti-emetic and analgesic effects, cannabinoids can inhibit tumor growth, survival and metastasis. The mechanisms of action of cannabinoids as anticancer agents are highly complex and not completely understood. Studies from our laboratory indicate that the specificity protein (Sp) transcription factors, Sp1, Sp3 and Sp4 that belong to the Sp/KLF family of transcription factors are overexpressed in many tumors and regulate critical factors responsible for cancer cell proliferation, growth, angiogenesis and survival. Hence, we hypothesized that cannabinoids elicit their responses on cancer cells by downregulating the expression of Sp proteins and Sp-regulated gene products. Treatment of colon and prostate cancer cells with the cannabinoids WIN and cannabidiol (CBD) inhibited cancer cell proliferation, induced apoptosis and downregulated Sp proteins and Sp-dependent genes. Furthermore, we demonstrated that WIN and CBD-mediated induction of apoptosis and repression of Sp proteins were mediated by phosphatases and that the phosphatase involved in WIN- dependent downregulation of Sp proteins was protein phosphatase 2A (PP2a). In addition WIN induced expression of ZBTB-10, an Sp repressor and downregulated microRNA-27a (miR27a) and these effects were PP2a-dependent indicating that WIN transcriptionally represses Sp protein expression by activating the phosphatase, PP2a. We also investigated the effects of 1,1-bis(3'-indolyl)-1-(p-bromophenyl)methan…
  note: by Sandeep Sreevalsan.
  note: "Major Subject: Toxicology"
  note: Includes vita.
  note: Doctor of Philosophy Texas A & M University 2013 http://hdl.handle.net/1969.1/151011
  note: Includes bibliographical references.
  note: Text (Dissertation)
  subject:
    topic: Major Toxicology
  subject:
    topic: Cancer
  subject:
    topic: Cannabinoids
  identifier: http://hdl.handle.net/1969.1/151011
  record info:
    record content source: TXA
    record creation date: 140303
    record change date: 20151206092222.0
    record identifier: in00003477435
    language of cataloging:
      language term: eng