乳腺癌患者的預後情況如何直接與腫瘤轉移的程度相關。然而，上皮型腫瘤細胞脫離原發腫瘤組織，轉移至遠端器官形成克隆轉移灶的確切機制至今不甚明了。
近來，刊登在The Journal of Biological Chemistry雜誌上的一則研究著重探究分析了乳腺癌腫瘤組織中垂體瘤轉化基因1（PTTG1）的表達水平，這個基因是一個相對未知的蛋白，研究人員將腫瘤患者源性乳房癌組織與相應的正常乳腺組織相比較，結果發現與正常組織相比，PTTG1高表達於乳腺癌患者中。
此外，PTTG1的表達水平與乳腺癌細胞株的惡性程度呈正相關性，遷移浸潤性能高的腫瘤細胞株MDA-MB-231和BT54高表達PTTG1，而遷移侵襲能力較弱的MCF7、SK- BR3以及正常MCF10A細胞株低表達PTTG1。
通過調控PTTG1的表達水平，研究人員發現PTTG1能通過調控上皮/間質細胞標誌物的表達、上調轉錄因子Snail來誘導上皮間質轉化，改變腫瘤細胞形態以提高乳腺癌細胞的遷移和侵襲特性。值得注意的是，PTTG1下調能通過減少腫瘤細胞自我更新能力和致瘤能力，抑制BT549細胞癌症幹細胞的數量，同時CD44高表達以及CD24低表達的細胞株數量也會降低，Sox2的表達也出現降低現象。
進一步研究證實PTTG1介導惡性腫瘤的特性部分是通過活化AKT來完成的，AKT是腫瘤細胞EMT和維持腫瘤細胞幹細胞樣特性的關鍵調節因子。總的來說，這些研究院結果表明PTTG1可能是一個惡性乳腺癌新的治療靶點。（生物谷：Bioon.com）
PTTG1 Oncogene Promotes Tumor Malignancy via Epithelial to Mesenchymal Transition and Expansion of Cancer Stem Cell Population*
Chang-Hwan Yoon, Min-Jung Kim, Hyejin Lee, Rae-Kwon Kim, Eun-Jung Lim, Ki-Chun Yoo,et al.
The prognosis of breast cancer patients is related to the degree of metastasis. However, the mechanisms by which epithelial tumor cells escape from the primary tumor and colonize at a distant site are not entirely understood. Here, we analyzed expression levels of pituitary tumor-transforming gene-1 (PTTG1), a relatively uncharacterized oncoprotein, in patient-derived breast cancer tissues with corresponding normal breast tissues. We found that PTTG1 is highly expressed in breast cancer patients, compared with normal tissues. Also, PTTG1 expression levels were correlated with the degree of malignancy in breast cancer cell lines; the more migratory and invasive cancer cell lines MDA-MB-231 and BT549 displayed the higher expression levels of PTTG1 than the less migratory and invasive MCF7 and SK-BR3 and normal MCF10A cell lines. By modulating PTTG1 expression levels, we found that PTTG1 enhances the migratory and invasive properties of breast cancer cells by inducing epithelial to mesenchymal transition, as evidenced by altered morphology and epithelial/mesenchymal cell marker expression patterns and up-regulation of the transcription factor Snail. Notably, down-regulation of PTTG1 also suppressed cancer stem cell population in BT549 cells by decreasing self-renewing ability and tumorigenic capacity, accompanying decreasing CD44high CD24low cells and Sox2 expression. Up-regulation of PTTG1 had the opposite effects, increasing sphere-forming ability and Sox2 expression. Importantly, PTTG1-mediated malignant tumor properties were due, at least in part, to activation of AKT, known to be a key regulator of both EMT and stemness in cancer cells. Collectively, these results suggest that PTTG1 may represent a new therapeutic target for malignant breast cancer.