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Targeting STAT Proteins for Cancer Therapy - Page 2

© David Olle

Researchers have found that STAT-3 activation helps cancer cells to evade the immune system. Studies have shown that STAT-3 signaling inhibits the maturation of dendritic cells, so that they are not functional. Additionally, the production of cytokines and chemokines are inhibited. As a result, T-cells tolerate the presence of cancer cells, and the immune system is not activated. 3

Cancer therapy based on STAT protein inhibition

Strategies to block STAT protein signaling in cancer cells do not appear to pose any problem in normal cells, even though STAT proteins are normal components in these cells as well. Cancer cells have developed a greater sensitivity and dependency to STAT proteins, so are more susceptible to destruction in their absence.

Studies are underway to determine the best approaches to blocking STAT proteins, which include inhibiting their formation, or disrupting their binding to DNA. 1 Antisense drugs block the expression of STAT protein genes. A gene therapy approach involves injecting DNA with a defective form of STAT protein into tumors. The DNA enters the nucleus of cancer cells, where it combines with the cellular DNA. Blocking STAT protein signaling may prove particularly beneficial in chemotherapy. The STAT dependent cancer cells could become more sensitive to chemotherapy, allowing less toxic, lower doses to be used.

References

1. Bowman, T., et. al. Signal transducers and activators of transcription: novel targets for anticancer therapeutics. Cancer Control, Vol. 6, No. 5, pp. 427-435 (1999)

2. Turksen, J. and Jove, R. STAT proteins: novel targets for cancer drug discovery. Oncogene, Vol. 19, No. 56, pp. 6613-6626 (Dec. 27, 2000)

3. Wang, T., et. al. Regulation of the innate and adaptive immune responses by STAT-3 signaling in tumor cells. Nature Medicine, Vol. 10, No. 1, pp.48-54 (Jan. 2004)

4. Yu, H. and Jove, R. The STATS of cancer-new molecular targets come of age. Nature Reviews Cancer, Vol. 4, No. 2, pp. 97-105 (Feb. 2004)

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