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PIM1 is responsible for IL-6-induced breast cancer cell EMT and stemness via c-myc activation.
Breast Cancer 2019; 26(5):663-671BC

Abstract

BACKGROUND

Interleukin-6 (IL-6) has been demonstrated to be a critical factor for breast cancer malignancy. However, the molecular mechanisms by which IL-6 induce breast cancer cells epithelial-mesenchymal-transition (EMT) and stemness remain elusive.

METHODS

Breast cancer cell lines T47D and MCF7 were exposed to IL-6, the expression of PIM1 was examined by quantitative real-time PCR (qRT-PCR) and western blot. Luciferase reporter assay was used to determine the transcriptional modulation of PIM1 by IL-6 and STAT3 inhibitor. Transwell assay was used to detect the invading ability of breast cancer cells induced by IL-6 or PIM1. The expressions of EMT and stemness markers were determined by qRT-PCR.

RESULTS

IL-6 promoted PIM1 expression in a dose- and time-dependent manner, and this induction could be abrogated by inhibiting STAT3 activation, subsequently suppressing the transcriptional level of PIM1. Moreover, we noticed that knocking down of PIM1 in cells which was exposed to IL-6 significantly impaired the invasion ability and the expression of EMT and stemness markers. On the contrary, overexpression of PIM1 promoted cell invasion and upregulated the expression of EMT and stemness markers. In addition, we demonstrated that c-myc, the cofactor of PIM1, involved in the pro-oncogenic roles of PIM1. Knocking down of c-myc attenuated the PIM1-induced cell EMT and stemness.

CONCLUSION

This study proposed the upregulation of PIM1 by IL-6 contributed to breast cancer cell aggressiveness and targeting PIM1 or c-myc could be novel approaches for breast cancer treatment.

Authors+Show Affiliations

Breast Disease Center, The Affiliated Hospital of Qingdao University, 59 Haier Road, Qingdao, 266000, Shandong, China.Medical Research Center, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266000, China.Department of Galactophore Surgery, Qingdao Women and Children's Hospital, Qingdao, Shandong, 266000, China.Breast Disease Center, The Affiliated Hospital of Qingdao University, 59 Haier Road, Qingdao, 266000, Shandong, China.Breast Disease Center, The Affiliated Hospital of Qingdao University, 59 Haier Road, Qingdao, 266000, Shandong, China.Breast Disease Center, The Affiliated Hospital of Qingdao University, 59 Haier Road, Qingdao, 266000, Shandong, China.Breast Disease Center, The Affiliated Hospital of Qingdao University, 59 Haier Road, Qingdao, 266000, Shandong, China.Breast Disease Center, The Affiliated Hospital of Qingdao University, 59 Haier Road, Qingdao, 266000, Shandong, China. seawangqd@126.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30989585

Citation

Gao, Xueqiang, et al. "PIM1 Is Responsible for IL-6-induced Breast Cancer Cell EMT and Stemness Via C-myc Activation." Breast Cancer (Tokyo, Japan), vol. 26, no. 5, 2019, pp. 663-671.
Gao X, Liu X, Lu Y, et al. PIM1 is responsible for IL-6-induced breast cancer cell EMT and stemness via c-myc activation. Breast Cancer. 2019;26(5):663-671.
Gao, X., Liu, X., Lu, Y., Wang, Y., Cao, W., Liu, X., ... Wang, H. (2019). PIM1 is responsible for IL-6-induced breast cancer cell EMT and stemness via c-myc activation. Breast Cancer (Tokyo, Japan), 26(5), pp. 663-671. doi:10.1007/s12282-019-00966-3.
Gao X, et al. PIM1 Is Responsible for IL-6-induced Breast Cancer Cell EMT and Stemness Via C-myc Activation. Breast Cancer. 2019;26(5):663-671. PubMed PMID: 30989585.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - PIM1 is responsible for IL-6-induced breast cancer cell EMT and stemness via c-myc activation. AU - Gao,Xueqiang, AU - Liu,Xiangping, AU - Lu,Yangyong, AU - Wang,Yu, AU - Cao,Weihong, AU - Liu,Xiaoyi, AU - Hu,Haiyan, AU - Wang,Haibo, Y1 - 2019/04/15/ PY - 2018/11/19/received PY - 2019/03/25/accepted PY - 2019/4/17/pubmed PY - 2019/4/17/medline PY - 2019/4/17/entrez KW - Breast cancer KW - EMT KW - IL-6 KW - PIM1 KW - c-Myc SP - 663 EP - 671 JF - Breast cancer (Tokyo, Japan) JO - Breast Cancer VL - 26 IS - 5 N2 - BACKGROUND: Interleukin-6 (IL-6) has been demonstrated to be a critical factor for breast cancer malignancy. However, the molecular mechanisms by which IL-6 induce breast cancer cells epithelial-mesenchymal-transition (EMT) and stemness remain elusive. METHODS: Breast cancer cell lines T47D and MCF7 were exposed to IL-6, the expression of PIM1 was examined by quantitative real-time PCR (qRT-PCR) and western blot. Luciferase reporter assay was used to determine the transcriptional modulation of PIM1 by IL-6 and STAT3 inhibitor. Transwell assay was used to detect the invading ability of breast cancer cells induced by IL-6 or PIM1. The expressions of EMT and stemness markers were determined by qRT-PCR. RESULTS: IL-6 promoted PIM1 expression in a dose- and time-dependent manner, and this induction could be abrogated by inhibiting STAT3 activation, subsequently suppressing the transcriptional level of PIM1. Moreover, we noticed that knocking down of PIM1 in cells which was exposed to IL-6 significantly impaired the invasion ability and the expression of EMT and stemness markers. On the contrary, overexpression of PIM1 promoted cell invasion and upregulated the expression of EMT and stemness markers. In addition, we demonstrated that c-myc, the cofactor of PIM1, involved in the pro-oncogenic roles of PIM1. Knocking down of c-myc attenuated the PIM1-induced cell EMT and stemness. CONCLUSION: This study proposed the upregulation of PIM1 by IL-6 contributed to breast cancer cell aggressiveness and targeting PIM1 or c-myc could be novel approaches for breast cancer treatment. SN - 1880-4233 UR - https://www.unboundmedicine.com/medline/citation/30989585/PIM1_is_responsible_for_IL-6-induced_breast_cancer_cell_EMT_and_stemness_via_c-myc_activation L2 - https://dx.doi.org/10.1007/s12282-019-00966-3 DB - PRIME DP - Unbound Medicine ER -