An increased awareness on a molecular level of what mechanisms prostate cancer cells use to become mobile and start spreading may, in the long run, provide new opportunities for treatment of aggressive prostate cancer. This is suggested by new results reported in a just-published study by researchers at Umeå University, Sweden, in collaboration with researchers in Uppsala, Sweden, and Tokyo, Japan. The study was published online on September 3, 2020 in iScience. The open-access article is titled “Smad7 Enhances TGF-β-Induced Transcription of c-Jun and HDAC6 Promoting Invasion of Prostate Cancer Cells.” (Se graphcial summary of article at end. “We can show that one specific amino acid in a signaling molecule plays an important role in mobilizing the cancer cells, and in that way increases the risk of metastases,” says Maréne Landström (photo), MD, PhD, Professor of Pathology, Umeå University. This research has studied the growth factor TGF-β (transforming growth factor beta), which regulates how cells grow and specialize. Previous studies have shown an overproduction of TGF-β in many forms of cancer, one being prostate cancer. High levels of TGF-β have proven to be strongly linked with poor prognosis and low survival rates as a consequence of the growth factor stimulating cancer cells to spread in the human body and cause life-threatening secondary tumors, so-called metastases. TGF-β regulates the expression of the protein Smad7--an active component in the TGF-β signaling chain. In healthy cells, Smad7 can prevent continued TGF-β signaling via negative feedback. However, Dr. Landström and her research group at Umeå University, and colleagues, have now shown, contrary to previous belief, that, in cancer cells, Smad7 can reinforce the development of tumors by regulating the gene expression of HDAC6 and c-Jun.
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