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Article

miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer

  • Authors:
    • Xiaomeng Dai
    • Mao Fang
    • Shuang Li
    • Yongrong Yan
    • Ying Zhong
    • Bin Du
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, Medical School of Jinan University, Guangzhou, Guangdong 510632, P.R. China, Department of Pathology, School of Basic Medical Science, Guangzhou Medical University, Guangzhou, Guangdong 510436, P.R. China
  • Pages: 6929-6936
    |
    Published online on: September 20, 2017
       https://doi.org/10.3892/ol.2017.7007
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Abstract

Transforming growth factor β1 (TGF‑β1) has been associated with poor outcomes in patients with breast cancer. However, the functions and underlying molecular mechanisms of TGF‑β1 in breast cancer remain unknown. Therefore, the present study aimed to identify the effects of components of the TGF‑β/microRNA (miR‑)21/phosphatase and tensin homolog (PTEN) signaling axis in breast cancer. TGF‑β1 was identified to upregulate the expression of miR‑21, and miR‑21 was demonstrated to be significantly upregulated in breast cancer tissues compared with benign proliferative breast disease. In addition, the expression of miR‑21 was significantly associated with increased TGF‑β1 and clinical characteristics in patients, including tumor grade and lymph node metastasis (all P<0.05). Furthermore, in the breast cancer MCF‑7 cell line, TGF‑β1 was revealed to induce the expression of miR‑21 in a dose‑ and time‑dependent manner. The results of the present study additionally demonstrated that increased miR‑21, in response to TGF‑β1 signaling, was associated with tumor invasion and chemoresistance in vitro. In addition, suppression of PTEN was mediated by TGF‑β1‑induced expression of miR‑21 in breast cancer cells and using a miR‑21 inhibitor revitalized the expression of PTEN. The results of the present study explored the functions of TGF‑β1‑stimulated expression of miR‑21 to suppress the PTEN axis, which promotes breast cancer progression and chemoresistance.
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Copy and paste a formatted citation
Spandidos Publications style
Dai X, Fang M, Li S, Yan Y, Zhong Y and Du B: miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer. Oncol Lett 14: 6929-6936, 2017.
APA
Dai, X., Fang, M., Li, S., Yan, Y., Zhong, Y., & Du, B. (2017). miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer. Oncology Letters, 14, 6929-6936. https://doi.org/10.3892/ol.2017.7007
MLA
Dai, X., Fang, M., Li, S., Yan, Y., Zhong, Y., Du, B."miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer". Oncology Letters 14.6 (2017): 6929-6936.
Chicago
Dai, X., Fang, M., Li, S., Yan, Y., Zhong, Y., Du, B."miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer". Oncology Letters 14, no. 6 (2017): 6929-6936. https://doi.org/10.3892/ol.2017.7007
Copy and paste a formatted citation
x
Spandidos Publications style
Dai X, Fang M, Li S, Yan Y, Zhong Y and Du B: miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer. Oncol Lett 14: 6929-6936, 2017.
APA
Dai, X., Fang, M., Li, S., Yan, Y., Zhong, Y., & Du, B. (2017). miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer. Oncology Letters, 14, 6929-6936. https://doi.org/10.3892/ol.2017.7007
MLA
Dai, X., Fang, M., Li, S., Yan, Y., Zhong, Y., Du, B."miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer". Oncology Letters 14.6 (2017): 6929-6936.
Chicago
Dai, X., Fang, M., Li, S., Yan, Y., Zhong, Y., Du, B."miR‑21 is involved in transforming growth factor β1‑induced chemoresistance and invasion by targeting PTEN in breast cancer". Oncology Letters 14, no. 6 (2017): 6929-6936. https://doi.org/10.3892/ol.2017.7007
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