Open Access

ISL1 promotes cancer progression and inhibits cisplatin sensitivity in triple-negative breast cancer cells

  • Authors:
    • Yang Zhang
    • Lu Wang
    • Peng Gao
    • Zhiguo Sun
    • Ning Li
    • Yanqin Lu
    • Jianglun Shen
    • Jian Sun
    • Yiming Yang
    • Hao Dai
    • Haifeng Cai
  • View Affiliations

  • Published online on: August 27, 2018     https://doi.org/10.3892/ijmm.2018.3842
  • Pages: 2343-2352
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Triple‑negative breast cancer (TNBC) is a type of breast cancer that is characterized by the lack of expression of estrogen and progesterone receptors, and epidermal growth factor receptor 2. Therefore, there is an absence of a specific target for effective therapy in TNBC. Cisplatin is usually employed as a first‑line chemotherapy agent for patients with TNBC. However, resistance remains an obstacle for cisplatin‑based chemotherapy, due to its elusive underlying mechanism. Previously, abnormal expression of Islet 1 (ISL1) was demonstrated to be closely associated with cancer development and progression. The present study revealed that (ISL1) was significantly upregulated in TNBC tissues in comparison with adjacent normal tissues. Overexpression of ISL1 markedly promoted the proliferation and invasion of the TNBC MDA‑MB‑231 and MDA‑MB‑468 cell lines, while knockdown of ISL1 inhibited cell invasion and proliferation in these cell lines. In addition, overexpression of ISL1 reversed cisplatin‑induced cell apoptosis, while knockdown of ISL1 enhanced apoptosis following cisplatin treatment in MDA‑MB‑231 and MDA‑MB‑468 cells. Furthermore, the levels of the anti‑apoptotic proteins, phosphorylated‑protein kinase B and B‑cell lymphoma‑2 (Bcl‑2), were significantly decreased, while the levels of the pro‑apoptotic protein Bcl‑2‑associated X protein were remarkably increased in response to cisplatin treatment. The present study revealed that ISL1 overexpression reversed the protein expression profile of p‑Akt, Bcl‑2 and Bax, while ISL1 knockdown promoted cell apoptosis. Therefore, the data of the present study demonstrated that ISL1 contributes to TNBC progression and reverses cell sensitivity towards cisplatin in TNBC cells, suggesting that ISL1 is a potential therapeutic target for the treatment of TNBC.
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November-2018
Volume 42 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Zhang Y, Wang L, Gao P, Sun Z, Li N, Lu Y, Shen J, Sun J, Yang Y, Dai H, Dai H, et al: ISL1 promotes cancer progression and inhibits cisplatin sensitivity in triple-negative breast cancer cells. Int J Mol Med 42: 2343-2352, 2018.
APA
Zhang, Y., Wang, L., Gao, P., Sun, Z., Li, N., Lu, Y. ... Cai, H. (2018). ISL1 promotes cancer progression and inhibits cisplatin sensitivity in triple-negative breast cancer cells. International Journal of Molecular Medicine, 42, 2343-2352. https://doi.org/10.3892/ijmm.2018.3842
MLA
Zhang, Y., Wang, L., Gao, P., Sun, Z., Li, N., Lu, Y., Shen, J., Sun, J., Yang, Y., Dai, H., Cai, H."ISL1 promotes cancer progression and inhibits cisplatin sensitivity in triple-negative breast cancer cells". International Journal of Molecular Medicine 42.5 (2018): 2343-2352.
Chicago
Zhang, Y., Wang, L., Gao, P., Sun, Z., Li, N., Lu, Y., Shen, J., Sun, J., Yang, Y., Dai, H., Cai, H."ISL1 promotes cancer progression and inhibits cisplatin sensitivity in triple-negative breast cancer cells". International Journal of Molecular Medicine 42, no. 5 (2018): 2343-2352. https://doi.org/10.3892/ijmm.2018.3842