Pituitary tumor-transforming gene 1 regulates invasion of prostate cancer cells through MMP13

Tumor Biology ◽  
2015 ◽  
Vol 37 (12) ◽  
pp. 15495-15500 ◽  
Author(s):  
Yun-Hua Lin ◽  
Yong Tian ◽  
Jun-Sheng Wang ◽  
Yong-Guang Jiang ◽  
Yong Luo ◽  
...  
Endocrinology ◽  
2003 ◽  
Vol 144 (11) ◽  
pp. 4991-4998 ◽  
Author(s):  
Run Yu ◽  
Wenge Lu ◽  
Jiandong Chen ◽  
Chris J. McCabe ◽  
Shlomo Melmed

Abstract The mammalian securin, pituitary tumor-transforming gene (PTTG), is overexpressed in several tumors and transforms cells in vitro and in vivo. To test the hypothesis that PTTG overexpression causes aneuploidy, enhanced green fluorescent protein (EGFP)-tagged PTTG (PTTG-EGFP) was expressed in human H1299 cancer cells (with undetectable endogenous PTTG expression) and mitosis of individual live cells observed. Untransfected cells and cells expressing EGFP alone exhibited appropriate mitosis. PTTG-EGFP markedly prolonged prophase and metaphase, indicating that PTTG blocks progression of mitosis to anaphase. In cells that underwent apparently normal mitosis (35 of 65 cells), PTTG-EGFP was degraded about 1 min before anaphase onset. Cells that failed to degrade PTTG-EGFP exhibited asymmetrical cytokinesis without chromosome segregation (18 of 65 cells) or chromosome decondensation without cytokinesis (9 of 65 cells), resulting in appearance of a macronucleus. Fifty-one of 55 cells expressing a nondegradable mutant PTTG exhibited asymmetrical cytokinesis without chromosome segregation, and some (4 of 55) decondensed chromosomes, both resulting in macronuclear formation. During this abnormal cytokinesis, all chromosomes and spindles and both centrosomes moved to one daughter cell, suggesting potential chaos in the subsequent mitosis. In conclusion, failure of PTTG degradation or enhanced PTTG accumulation, as a consequence of overexpression, inhibits mitosis progression and chromosome segregation but does not directly affect cytokinesis, resulting in aneuploidy. These results demonstrate that PTTG induces aneuploidy in single, live, human cancer cells.


Tumor Biology ◽  
2015 ◽  
Vol 37 (12) ◽  
pp. 15567-15573 ◽  
Author(s):  
Lin Li ◽  
Li-Ying Han ◽  
Ming Yu ◽  
Qi Zhou ◽  
Jian-Cheng Xu ◽  
...  

2011 ◽  
Vol 50 (9) ◽  
pp. 655-667 ◽  
Author(s):  
Sudhakar Chintharlapalli ◽  
Sabitha Papineni ◽  
Syng-Ook Lee ◽  
Ping Lei ◽  
Un Ho Jin ◽  
...  

2013 ◽  
Vol 35 ◽  
pp. 267-272 ◽  
Author(s):  
Fabio Grizzi ◽  
Sonia Di Biccari ◽  
Barbara Fiamengo ◽  
Sanja Štifter ◽  
Piergiuseppe Colombo

Despite the advances that have been made in the fields of molecular and cell biology, there is still considerable debate explaining how the breast cancer cells progress through carcinogenesis and acquire their metastatic ability. The lack of preventive methods and effective therapies underlines the pressing need to identify new biomarkers that can aid early diagnosis and may be targets for effective therapeutic strategies. In this study we explore the pituitary tumor-transforming gene 1 (PTTG1) expression in primary ductal breast carcinoma, lymph node infiltration, and distant metastases. Three human cell lines, 184B5 derived from normal mammary epithelium, HCC70 from a primary ductal carcinoma, and MDA-MB-361 from a breast metastasis, were used for quantifying PTTG1 mRNA expression. The PTTG1 immunohistochemical expression was carried out on specimens taken from eight patients with invasive ductal breast cancer who underwent surgical treatment and followup for five years retrospectively selected. The study demonstrated that PTTG1 is expressed gradually in primary ductal breast carcinoma, lymph node infiltration, and distant metastases. Our findings suggest that the immunohistochemical evaluation of PTTG1 expression might be a powerful biomarker of recognition and quantification of the breast cancer cells in routine pathological specimens and a potential target for developing an effective immunotherapeutic strategy for primary and metastatic breast cancer.


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