HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway

Research output: Contribution to journalArticle

Yi Liu, Dong Soon Choi, Jianting Sheng, Joe E. Ensor, Diana Hwang Liang, Cristian Rodriguez-Aguayo, Amanda Polley, Steve Benz, Olivier Elemento, Akanksha Verma, Yang Cong, Helen Wong, Wei Qian, Zheng Li, Sergio Granados-Principal, Gabriel Lopez-Berestein, Melissa D. Landis, Roberto R. Rosato, Bhuvanesh Dave, Stephen Wong & 3 others Dario Marchetti, Anil K. Sood, Jenny C. Chang

Here, we show that HEMATOLOGICAL AND NEUROLOGICAL EXPRESSED 1-LIKE (HN1L) is a targetable breast cancer stem cell (BCSC) gene that is altered in 25% of whole breast cancer and significantly correlated with shorter overall or relapse-free survival in triple-negative breast cancer (TNBC) patients. HN1L silencing reduced the population of BCSCs, inhibited tumor initiation, resensitized chemoresistant tumors to docetaxel, and hindered cancer progression in multiple TNBC cell line-derived xenografts. Additionally, gene signatures associated with HN1L correlated with shorter disease-free survival of TNBC patients. We defined HN1L as a BCSC transcription regulator for genes involved in the LEPR-STAT3 signaling axis as HN1L binds to a putative consensus upstream sequence of STAT3, LEPTIN RECEPTOR, and MIR-150. Our data reveal that BCSCs in TNBC depend on the transcription regulator HN1L for the sustained activation of the LEPR-STAT3 pathway, which makes it a potentially important target for both prognosis and BCSC therapy. Yi et al. describe HN1L as a novel transcription regulator for breast cancer stem cells (BCSCs) in triple-negative breast cancer (TNBC), promoting LEPR and miR-150 expression and activating the STAT3 pathway. Since BCSCs contribute to chemoresistance and metastasis in TNBC, further investigation of HN1L will offer new therapeutic strategies.

Original languageEnglish (US)
JournalStem Cell Reports
Early online dateDec 8 2017
DOIs
StateE-pub ahead of print - Dec 8 2017

PMID: 29249663

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HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway. / Liu, Yi; Choi, Dong Soon; Sheng, Jianting; Ensor, Joe E.; Liang, Diana Hwang; Rodriguez-Aguayo, Cristian; Polley, Amanda; Benz, Steve; Elemento, Olivier; Verma, Akanksha; Cong, Yang; Wong, Helen; Qian, Wei; Li, Zheng; Granados-Principal, Sergio; Lopez-Berestein, Gabriel; Landis, Melissa D.; Rosato, Roberto R.; Dave, Bhuvanesh; Wong, Stephen; Marchetti, Dario; Sood, Anil K.; Chang, Jenny C.

In: Stem Cell Reports, 08.12.2017.

Research output: Contribution to journalArticle

Harvard

Liu, Y, Choi, DS, Sheng, J, Ensor, JE, Liang, DH, Rodriguez-Aguayo, C, Polley, A, Benz, S, Elemento, O, Verma, A, Cong, Y, Wong, H, Qian, W, Li, Z, Granados-Principal, S, Lopez-Berestein, G, Landis, MD, Rosato, RR, Dave, B, Wong, S, Marchetti, D, Sood, AK & Chang, JC 2017, 'HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway' Stem Cell Reports. https://doi.org/10.1016/j.stemcr.2017.11.010

APA

Liu, Y., Choi, D. S., Sheng, J., Ensor, J. E., Liang, D. H., Rodriguez-Aguayo, C., ... Chang, J. C. (2017). HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway. Stem Cell Reports. https://doi.org/10.1016/j.stemcr.2017.11.010

Vancouver

Liu Y, Choi DS, Sheng J, Ensor JE, Liang DH, Rodriguez-Aguayo C et al. HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway. Stem Cell Reports. 2017 Dec 8. https://doi.org/10.1016/j.stemcr.2017.11.010

Author

Liu, Yi ; Choi, Dong Soon ; Sheng, Jianting ; Ensor, Joe E. ; Liang, Diana Hwang ; Rodriguez-Aguayo, Cristian ; Polley, Amanda ; Benz, Steve ; Elemento, Olivier ; Verma, Akanksha ; Cong, Yang ; Wong, Helen ; Qian, Wei ; Li, Zheng ; Granados-Principal, Sergio ; Lopez-Berestein, Gabriel ; Landis, Melissa D. ; Rosato, Roberto R. ; Dave, Bhuvanesh ; Wong, Stephen ; Marchetti, Dario ; Sood, Anil K. ; Chang, Jenny C. / HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway. In: Stem Cell Reports. 2017.

BibTeX

@article{5811b179116c4497bba8ffb331f19ac2,
title = "HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway",
abstract = "Here, we show that HEMATOLOGICAL AND NEUROLOGICAL EXPRESSED 1-LIKE (HN1L) is a targetable breast cancer stem cell (BCSC) gene that is altered in 25{\%} of whole breast cancer and significantly correlated with shorter overall or relapse-free survival in triple-negative breast cancer (TNBC) patients. HN1L silencing reduced the population of BCSCs, inhibited tumor initiation, resensitized chemoresistant tumors to docetaxel, and hindered cancer progression in multiple TNBC cell line-derived xenografts. Additionally, gene signatures associated with HN1L correlated with shorter disease-free survival of TNBC patients. We defined HN1L as a BCSC transcription regulator for genes involved in the LEPR-STAT3 signaling axis as HN1L binds to a putative consensus upstream sequence of STAT3, LEPTIN RECEPTOR, and MIR-150. Our data reveal that BCSCs in TNBC depend on the transcription regulator HN1L for the sustained activation of the LEPR-STAT3 pathway, which makes it a potentially important target for both prognosis and BCSC therapy. Yi et al. describe HN1L as a novel transcription regulator for breast cancer stem cells (BCSCs) in triple-negative breast cancer (TNBC), promoting LEPR and miR-150 expression and activating the STAT3 pathway. Since BCSCs contribute to chemoresistance and metastasis in TNBC, further investigation of HN1L will offer new therapeutic strategies.",
keywords = "Cancer stem cells, HN1L, LEPR, STAT3, TNBC",
author = "Yi Liu and Choi, {Dong Soon} and Jianting Sheng and Ensor, {Joe E.} and Liang, {Diana Hwang} and Cristian Rodriguez-Aguayo and Amanda Polley and Steve Benz and Olivier Elemento and Akanksha Verma and Yang Cong and Helen Wong and Wei Qian and Zheng Li and Sergio Granados-Principal and Gabriel Lopez-Berestein and Landis, {Melissa D.} and Rosato, {Roberto R.} and Bhuvanesh Dave and Stephen Wong and Dario Marchetti and Sood, {Anil K.} and Chang, {Jenny C.}",
year = "2017",
month = "12",
day = "8",
doi = "10.1016/j.stemcr.2017.11.010",
language = "English (US)",
journal = "Stem Cell Reports",
issn = "2213-6711",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - HN1L Promotes Triple-Negative Breast Cancer Stem Cells through LEPR-STAT3 Pathway

AU - Liu, Yi

AU - Choi, Dong Soon

AU - Sheng, Jianting

AU - Ensor, Joe E.

AU - Liang, Diana Hwang

AU - Rodriguez-Aguayo, Cristian

AU - Polley, Amanda

AU - Benz, Steve

AU - Elemento, Olivier

AU - Verma, Akanksha

AU - Cong, Yang

AU - Wong, Helen

AU - Qian, Wei

AU - Li, Zheng

AU - Granados-Principal, Sergio

AU - Lopez-Berestein, Gabriel

AU - Landis, Melissa D.

AU - Rosato, Roberto R.

AU - Dave, Bhuvanesh

AU - Wong, Stephen

AU - Marchetti, Dario

AU - Sood, Anil K.

AU - Chang, Jenny C.

PY - 2017/12/8

Y1 - 2017/12/8

N2 - Here, we show that HEMATOLOGICAL AND NEUROLOGICAL EXPRESSED 1-LIKE (HN1L) is a targetable breast cancer stem cell (BCSC) gene that is altered in 25% of whole breast cancer and significantly correlated with shorter overall or relapse-free survival in triple-negative breast cancer (TNBC) patients. HN1L silencing reduced the population of BCSCs, inhibited tumor initiation, resensitized chemoresistant tumors to docetaxel, and hindered cancer progression in multiple TNBC cell line-derived xenografts. Additionally, gene signatures associated with HN1L correlated with shorter disease-free survival of TNBC patients. We defined HN1L as a BCSC transcription regulator for genes involved in the LEPR-STAT3 signaling axis as HN1L binds to a putative consensus upstream sequence of STAT3, LEPTIN RECEPTOR, and MIR-150. Our data reveal that BCSCs in TNBC depend on the transcription regulator HN1L for the sustained activation of the LEPR-STAT3 pathway, which makes it a potentially important target for both prognosis and BCSC therapy. Yi et al. describe HN1L as a novel transcription regulator for breast cancer stem cells (BCSCs) in triple-negative breast cancer (TNBC), promoting LEPR and miR-150 expression and activating the STAT3 pathway. Since BCSCs contribute to chemoresistance and metastasis in TNBC, further investigation of HN1L will offer new therapeutic strategies.

AB - Here, we show that HEMATOLOGICAL AND NEUROLOGICAL EXPRESSED 1-LIKE (HN1L) is a targetable breast cancer stem cell (BCSC) gene that is altered in 25% of whole breast cancer and significantly correlated with shorter overall or relapse-free survival in triple-negative breast cancer (TNBC) patients. HN1L silencing reduced the population of BCSCs, inhibited tumor initiation, resensitized chemoresistant tumors to docetaxel, and hindered cancer progression in multiple TNBC cell line-derived xenografts. Additionally, gene signatures associated with HN1L correlated with shorter disease-free survival of TNBC patients. We defined HN1L as a BCSC transcription regulator for genes involved in the LEPR-STAT3 signaling axis as HN1L binds to a putative consensus upstream sequence of STAT3, LEPTIN RECEPTOR, and MIR-150. Our data reveal that BCSCs in TNBC depend on the transcription regulator HN1L for the sustained activation of the LEPR-STAT3 pathway, which makes it a potentially important target for both prognosis and BCSC therapy. Yi et al. describe HN1L as a novel transcription regulator for breast cancer stem cells (BCSCs) in triple-negative breast cancer (TNBC), promoting LEPR and miR-150 expression and activating the STAT3 pathway. Since BCSCs contribute to chemoresistance and metastasis in TNBC, further investigation of HN1L will offer new therapeutic strategies.

KW - Cancer stem cells

KW - HN1L

KW - LEPR

KW - STAT3

KW - TNBC

UR - http://www.scopus.com/inward/record.url?scp=85039056430&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85039056430&partnerID=8YFLogxK

U2 - 10.1016/j.stemcr.2017.11.010

DO - 10.1016/j.stemcr.2017.11.010

M3 - Article

JO - Stem Cell Reports

T2 - Stem Cell Reports

JF - Stem Cell Reports

SN - 2213-6711

ER -

ID: 38662673