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Inhibition of ErbB‐2 induces TFF 3 downregulation in breast cancer cell lines
Author(s) -
Yue Lu,
Xiang Jinyu,
Shen Zan,
Wang Zhihao,
Yao Yasai,
Zhou Quan,
Ding Aiping,
Qiu Wensheng
Publication year - 2014
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/apm.12203
Subject(s) - breast cancer , downregulation and upregulation , erbb , immunohistochemistry , blot , gene silencing , breast carcinoma , cancer research , medicine , cancer , pathology , biology , gene , biochemistry
ErbB‐2 gene plays an important role in carcinoma formation whose overexpression was observed in many types of tumors, including breast cancer. Dysregulation of Trefoil factor 3 ( TFF 3), which is thought to function in the development and progression of breast cancer, was found to be upregulated in ErbB2‐overexpressing breast cancers and cells. However, a putative interaction between ErbB‐2 and TFF 3 in breast cancer remains unknown. To determine whether TFF 3 has an important role in breast tumor, its levels were measured by immunohistochemistry in 130 cases of breast infiltrating duct carcinoma and 30 cases of normal breast tissue with a specific monoclonal antibody raised against human TFF 3. Patients who were positive for ErbB‐2 also had high expression levels of TFF 3 (p < 0.05). Also, after infecting the SK ‐ BR ‐3 cells with lentivirus‐mediated ErbB2‐specific sh RNA (Lenti‐Sh ERBB 2), we detected the expressions of ErbB‐2 and TFF 3 by real‐time polymerase chain reaction and Western blotting, respectively. Compared with the control groups, ErbB‐2 m RNA expression was decreased in the Lenti‐Sh ERBB 2 infection group, and Western blotting indicated a concordant ErbB‐2 protein reduction. On the other hand, TFF 3 expression at both m RNA and protein levels was significantly downregulated by ErbB‐2 silencing in SK ‐ BR ‐3. These findings are a proof of the foundation for a certain relationships of ErbB‐2 and TFF 3, which may serve as novel therapeutic markers of ErbB2‐overexpressing breast cancers in the future.