信号转导和转录激活因子3（STAT3）是涉及多种基本生物学过程的转录因子，也是癌症发展和进展的关键因素。STAT3在酪氨酸磷酸化后被激活，在各种恶性肿瘤中具有固有活性。因此，pSTAT3的表达已被认为是预测不良生存率的因素。STAT3编码两种不同剪接的STAT3亚型：全长度STAT3α亚型和截短的STAT3β亚型。这些亚型被认为是STAT3在癌症中有时扮演对立角色的原因：一方面是癌基因，另一方面是肿瘤抑制因子。为了探究它们在侵袭性乳腺癌中的作用，我们分别沉默了每种亚型，并发现它们影响彼此的激活，影响细胞生存能力、细胞因子表达和迁移。沉默特定的ISO型可以在细胞中导致更有利的激活STAT3蛋白质平衡。区分这两种亚型及其活性形式对于STAT3相关的癌症诊断和治疗非常重要。

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'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.