Monday, November 16, 2009

Growth inhibition of human ovarian cancer cells with siRNA

The article “Growth inhibition of human ovarian cancer cells by blocking STAT3 activation with small interfering RNA” by Liying Cai a, Guangmei Zhang et al. was accepted into the European Journal of Obstetrics & Gynecology and Reproductive Biology in September 2009. According to the article taken from ScienceDirect, ovarian cancer is the cause of approximately 125,000 deaths per year in the developed world. Furthermore, less than one third of the ovarian cancer patients are able to survive long term. According to Doctor Frederick Sweet from Washington University School of Medicine, there are currently several therapies for ovarian cancer, including, but not limited to, surgery and chemotherapy (1) . However, ovarian cancer can at times become easily resistant to these therapies or some “current therapies for advanced ovarian cancer are not effective enough (2)."
As a result, this article demonstrates the potential application of RNA interference as a new class of therapeutic under the scope of personalized medicine. RNA interference would be used in tumor therapy as an inhibitor of transcription 3 pathway (STAT3); the overexpressed STAT3, when active, is known to “contribute to tumorigenesis in ovarian cancer (3).” The journal article demonstrates that not only does siRNA act as an inhibitor of STAT3 cell proliferation, but also “STAT3-siRNA treatment [obviously] increased the percentage of apoptotic (death of ovarian cancer cells) cells (4)”—both highly necessary to efficiently treat cancer.
However, one must keep in mind that this study tested the inhibitor effect siRNA had on STAT3 invitro. In this preliminary stage, the study demonstrates that siRNA could potentially become a therapy for human ovarian cancer; however, more tests have yet to come to prove the efficacy of the siRNA as an inhibitor in actual patients with ovarian cancer. Nonetheless, it is important to note that there are other studies providing information on the potential benefits STAT3 inhibition, through the use of small RNA molecules, has on treating breast cancer(5) , human colon cancer (6) , etc. Therefore, as current cancer therapies’ effectiveness rates come short from meeting patients’ expectations and articles such as this one provide hope, the stronger the support and positive perception the public will have towards advancements in the use of small RNA molecules in cancer research and future treatment.
For more information go to: http://dx.doi.org and enter the following entire DOI citation in the text box provided doi:10.1016/j.ejogrb.2009.09.018

Footnotes
(1)- http://www.thedoctorwillseeyounow.com/articles/womens_health/ovarian_18/
(2)- Cai L, et al. Growth inhibition of human ovarian cancer cells by blocking STAT3 activation with small
interfering RNA. Eur J Obstet Gynecol (2009), doi:10.1016/j.ejogrb.2009.09.018
(3)- C.N. Landen Jr., Y.G. Lin and G.N. Armaiz Pena et al., Neuroendocrine modulation of signal transducer and activator of transcription-3 in ovarian cancer, Cancer Res 67 (2007), pp. 10389–10396
(4)- Cai L, et al. Growth inhibition of human ovarian cancer cells by blocking STAT3 activation with small
interfering RNA. Eur J Obstet Gynecol (2009), doi:10.1016/j.ejogrb.2009.09.018
(5)- Xiaoyang Ling and Ralph B. Arlinghaus, Knockdown of STAT3 Expression by RNA Interference Inhibits the Induction of Breast Tumors in Immunocompetent Mice, Cancer Research 65, 2532-2536, April 1, 2005
(6)- Yu Fan, You-Li Zhang et al., Inhibition of signal transducer and activator of transcription 3 expression by RNA interference suppresses invasion through inducing anoikis in human colon cancer cells, World J Gastroenterol. 2008 January 21; 14(3): 428–434.

1 comment:

  1. Thank you for posting this! I thought this article referencing use of i-Fect siRNA delivery reagent could be of interest to readers:
    Joseph George, Naren L. Banik, Swapan K. Ray. Combination of hTERT Knockdown and IFN-γ Treatment Inhibited Angiogenesis and Tumor Progression in Glioblastoma. Clin Cancer Res 2009;15(23):7186–95

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