|
|
|
| Expression of signal transducer and activators of transcription 3 and Twist basic helix-loop-helix transcription factor 1 in epithelial ovarian cancer |
| HONG Li1▲ YANG Jiang1▲ XING Hui2 LU Danhua1 TANG Jianming1 LI Bingshu1 GUO Fengqin1 |
1.Department Ⅱ of Gynecology, Renmin Hospital of Wuhan University, Hubei Province, Wuhan 430060, China;
2.Department of Gynecology and Obstetrics, Xiangyang Central Hospital, Hubei Province, Xiangyang 441021, China |
|
|
|
Abstract Objective To investigate the expression of signal transducer and activators of transcription 3 (STAT3) and Twist basic helix-loop-helix transcription factor 1(Twist1) in epithelial ovarian cancer, and to analyze the relationship between the expression dysregulation and the occurrence and development of ovarian cancer. Methods The tissue of 49 cases with epithelial ovarian cancer and 14 cases with ovarian benign tumor taken surgery in Renmin Hospital of Wuhan University from March 2015 to December 2016 were collected. The expression of STAT3 and Twist1 protein was examined by immunohistochemistry streptavidin peroxidase conjugated method, the expression differences of which in early ovarian cancer and advanced ovarian cancer were compared and analyzed by Pearson correlation analysis. Results The positive expression rates of STAT3 and Twist1 in ovarian cancer were significantly higher than those of ovarian benign tumor, the differences were statistically significant (P ＜ 0.05). The positive expression rates of STAT3 and Twist1 in the advanced ovarian cancer were higher than those of early ovarian cancer, the differences were statistically significant (P ＜ 0.05). The positive expression of Twist1 in early ovarian cancer and advanced ovarian cancer was both positively correlated with STAT3(r = 0.653, 0.798, all P ＜ 0.05). Conclusion The expression of STAT3 and Twist1 plays an important role in the occurrence, development and deterioration of ovarian cancer, the positive expression rate has correlation with FIGO stage of ovarian cancer, and the mechanism may be achieved through epithelial-mesenehymal transition.
|
|
|
|
|
|
[1] Siegel R，Ma J，Zou Z，et al. Cancer statistics，2014 [J]. CA Cancer J Clin，2014，64（1）：9-29.
[2] Avtanski DB，Nagalingam A，Bonner MY，et al. Honokiol inhibits epithelial-mesenchymal transition in breast cancer cells by targeting signal transducer and activator of transcription 3/Zeb1/E-cadherin axis [J]. Mol Oncol，2014，8（3）：565-580.
[3] Britton KM，Kirby JA，Lennard TW，et al. Cancer stem cells and side population cells in breast cancer and metastasis [J]. Cancers（Basel），2011，3（2）：2106-2130.
[4] 钟宝元.大肠癌中STAT3、Twist的表达及与EMT关系的研究[J].中国医学创新，2014，11（36）：33-34.
[5] 于萍，步宏，王华，等.免疫组化结果的图像分析与人工计数方法的对比研究[J].生物医学工程学杂志，2003，20（2）：288-290.
[6] Bromberg JF，Wrzeszesczynska MH，Devgan G，et al. Stat3 as an oncogene [J]. Cell，1999，98（3）：295-303.
[7] Chai EZ，Shanmugam MK，Arfuso F，et al. Targeting transcription factor STAT3 for cancer prevention and therapy [J]. Pharmacol Ther，2016，162：86-97.
[8] Takeda K，Noguchi K，Shi W，et al. Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality [J]. Proc Natl Acad Sci USA，1997，94（8）：3801-3804.
[9] Shodeinde A，Ginjupalli K，Lewis HD，et al. STAT3 Inhibition Induces Apoptosis in Cancer Cells Independent of STAT1 or STAT2 [J]. J Mol Biochem，2013，2（1）：18-26.
[10] Zhang X，Liu P，Zhang B，et al. Inhibitory effects of STAT3 decoy oligodeoxynucleotides on human epithelial ovarian cancer cell growth in vivo [J]. Int J Mol Med，2013，32（3）：623-628.
[11] Morikawa T，Baba Y，Yamauchi M，et al. STAT3 expression，molecular features，inflammation patterns，and prognosis in a database of 724 colorectal cancers [J]. Clin Cancer Res，2011，17（6）：1452-1462.
[12] Thiery JP，Lim CT. Tumor dissemination：an EMT affair [J]. Cancer Cell，2013，23（3）：272-273.
[13] Scheel C，Weinberg RA. Cancer stem cells and epithelial-mesenchymal transition：concepts and molecular links [J]. Semin Cancer Biol，2012，22（5/6）：396-403.
[14] Khan MA，Chen H，Zhang D，et al. Twist：a molecular target in cancer therapeutics [J]. Tumour Biol，2013，34（5）：2497-2506.
[15] Howard TD，Paznekas WA，Green ED，et al. Mutations in TWIST，a basic helix-loop-helix transcription factor，in Saethre-Chotzen syndrome [J]. Nat Genet，1997，15（1）：36-41.
[16] Peinado H，Olmeda D，Cano A. Snail，Zeb and bHLH factors in tumour progression：an alliance against the epithelial phenotype? [J]. Nat Rev Cancer，2007，7（6）：415-428.
[17] Yu L，Lu S，Tian J，et al. TWIST expression in hypopharyngeal cancer and the mechanism of TWIST-induced promotion of metastasis [J]. Oncol Rep，2012，27（2）：416-422.
[18] Beck B，Lapouge G，Rorive S，et al. Different levels of Twist1 regulate skin tumor initiation，stemness，and progression [J]. Cell Stem Cell，2015，16（1）：67-79.
[19] Luo GQ，Li JH，Wen JF，et al. Effect and mechanism of the Twist gene on invasion and metastasis of gastric carcinoma cells [J]. World J Gastroenterol，2008，16（14）：2487-2493.
[20] Zhuo X，Chang A，Huang C，et al. Expression of TWIST，an inducer of epithelial-mesenchymal transition，in nasopharyngeal carcinoma and its clinical significance [J]. Int J Clin Exp Pathol，2014，7（12）：8862-8868.
[21] Yang J，Mani SA，Donaher JL，et al. Twist，a master regulator of morphogenesis，plays an essential role in tumor metastasis [J]. Cell，2004，117（7）：927-939.
[22] Hsu KW，Hsieh RH，Huang KH，et al. Activation of the Notch1/STAT3/Twist signaling axis promotes gastric cancer progression [J]. Carcinogenesis，2012，33（8）：1459-1467.
[23] Cheng GZ，Zhang WZ，Sun M，et al. Twist is transcriptionally induced by activation of STAT3 and mediates STAT3 oncogenic function [J]. J Biol Chem，2008，283（21）：14665-14673.
[24] Zhang CH，Xu GL，Jia WD，et al. Activation of STAT3 signal pathway correlates with twist and E-cadherin expression in hepatocellular carcinoma and their clinical significance [J]. J Surg Res，2012，174（1）：120-129. |
|
|
|
