Skip NavigationSkip to Content

NO and hepatocellular cancer

  1. Author:
    Wang, Ronghua
    Geller, David A.
    Wink,David
    Cheng, Bin
    Billiar, Timothy R.
  2. Author Address

    Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept Gastroenterol & Hepatol, Wuhan, Hubei, Peoples R China.Univ Pittsburgh, Sch Med, Dept Surg, Pittsburgh, PA 15213 USA.NCI, Canc Inflammat Program, NIH, Frederick, MD 21701 USA.
    1. Year: 2019
    2. Date: Dec 11
    3. Epub Date: 2019 08 18
  1. Journal: British journal of pharmacology
  2. WILEY,
  3. Type of Article: Review
  4. ISSN: 0007-1188
  1. Abstract:

    NO has broad and sometimes dichotomous roles in cancer. The effects of NO in tumours depend on the type and localization of NOS isoforms, concentration and duration of NO exposure, and cellular sensitivity to NO. Hepatocellular carcinoma (HCC) is a common and lethal disease for which no effective therapy other than sur4gical resection exists. Over two decades of research has yielded evidence that NO generated by the inducible NOS (iNOS or NOS2) contributes to HCC progression in at least a subset of patients with HCC. The co-expression of iNOS with COX-2 may portend a particularly aggressive cancer phenotype in HCC and at the same time reveal an opportunity for pharmacological intervention. In this review, we focus on what is known about the influence of NO in HCC neoplastic transformation, proliferation and apoptosis, angiogenesis, invasion, and metastasis, cancer stem cells, and the host immune response against the tumour. We discuss the implications of recent findings for targeting the NO pathways in HCC.

    See More

External Sources

  1. DOI: 10.1111/bph.14838
  2. PMID: 31423564
  3. WOS: 000502240900001

Library Notes

  1. Fiscal Year: FY2019-2020
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel