Skip to main content
padlock icon - secure page this page is secure

S3I-201, a Novel STAT3 Inhibitor, Inhibits Growth of Human Soft Tissue Sarcoma Cell Lines

Buy Article:

$107.19 + tax (Refund Policy)

Background: STAT3 has been identified as a novel target to treat and prevent cancers with a broad potential application. Aim: To investigate whether constitutive STAT3 plays a role in the survival and growth of soft tissue sarcoma (STS) cell lines. Materials and Methods: Expression and activity of STAT3 were characterized by Western blot and Immunohistochemistry staining. S3I-201 in different doses or vehicle was added into cell culture respectively. Cell growth and colony formation were determined using crystal violet colorimetric and clonogenic assays. Results: Western blot demonstrated 5 out of 6 STS cell lines expressed constitutively activated STAT3. STAT3 inhibitor S3I-201 mono-therapy induced anti-proliferative effects on majority of STS cell lines harboring aberrant STAT3 by blocking STAT3 phosphorylation. Conclusion: Our study demonstrated that a high level of STAT3 phosphorylation is present in the human STS cell lines that we examined. Furthermore targeting STAT3 is a potential novel approach to pursue in anti-sarcoma therapy.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
No Metrics

Keywords: CONSTITUTIVE ACTIVATION OF STAT3; S3I-201; SOFT TISSUE SARCOMA; STAT3 INHIBITION

Document Type: Research Article

Publication date: April 1, 2013

More about this publication?
  • World Journal of Cancer Research publishes original articles describing significant new findings in any area related to basic and clinical cancer research. These include studies of cancer related genes, molecules, drugs, cancer cell lines, tumorigenesis, cancer prevention, cancer progression and metastasis, cancer diagnosis, cancer treatment, cancer animal models, human cancer samples as well as cancer patients and all other cancer research related areas.
  • Editorial Board
  • Information for Authors
  • Subscribe to this Title
  • Aims and Scope
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more