@article{ad3bedd8c11547bea339eecb716d730c,
title = "Differential silencing of STAT3 isoforms leads to changes in STAT3 activation",
abstract = "Signal transducer and activator of transcription 3 (STAT3) is a transcription factor involved in multiple fundamental biological processes and a key player in cancer development and progression. STAT3 is activated upon tyrosine phosphorylation and is constitutively active in various malignancies; therefore, the expression of pSTAT3 has been recognized as a predictor of poor survival. STAT3 encodes two alternatively-spliced STAT3 isoforms: the full-length STAT3α isoform and the truncated STAT3β isoform. These isoforms have been suggested as the reason for the occasionally observed opposing roles of STAT3 in cancer: an oncogene, on one hand, and a tumor suppressor on the other. To investigate their roles in aggressive breast cancer, we separately silenced each isoform and found that they affect each other{\textquoteright}s activation, impacting cell viability, cytokine expression, and migration. Silencing specific isoforms can lead to a more favorable balance of activated STAT3 proteins in the cell. Distinguishing between the two isoforms and their active forms is crucial for STAT3-related cancer diagnosis and therapy.",
keywords = "STAT3, STAT3 isoforms, breast cancer, cancer diagnosis, cancer therapy",
author = "Inbal Shamir and Ilan Tsarfaty and Gidi Paret and Yael Nevo-Caspi",
note = "Publisher Copyright: Copyright: {\textcopyright} 2023 Shamir et al.",
year = "2023",
doi = "10.18632/oncotarget.28412",
language = "אנגלית",
volume = "14",
pages = "366--376",
journal = "Oncotarget",
issn = "1949-2553",
publisher = "Impact Journals LLC",
number = "1",
}