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Science China Life Sciences

, Volume 62, Issue 9, pp 1229–1242 | Cite as

C1orf106, an innate immunity activator, is amplified in breast cancer and is required for basal-like/luminal progenitor fate decision

  • Ji Ma
  • Cheng Liu
  • Decao Yang
  • Jiagui Song
  • Jing Zhang
  • Tianzhuo Wang
  • Mengyuan Wang
  • Weizhi Xu
  • Xueying Li
  • Shigang DingEmail author
  • Jun ZhanEmail author
  • Hongquan ZhangEmail author
Research Paper
  • 27 Downloads

Abstract

Basal-like breast cancer with a luminal progenitor gene expression profile is an aggressive subtype of breast cancer with a poorer prognosis compared with other subtypes. However, genes that specifically promote basal-like breast cancer development remain largely unknown. Here, we report that a novel gene C1orf106 plays an important role in maintaining the feature of basal-like/luminal progenitors. C1orf106 is frequently amplified and overexpressed in basal-like breast cancer and is associated with a poor outcome in patients. In human TCGA database, C1orf106 expression was correlated with upregulation of ELF5 and downregulation of GATA3, two transcription factors that regulate mammary gland stem cell fate. Enhanced expression of C1orf106 promotes tumor progression and expression of basal-like/luminal progenitor marker ELF5; depletion of C1orf106 suppresses tumorigenesis and expression of basal-like/luminal progenitor marker GATA3. These findings suggest that C1orf106 maintains the basal-like/luminal progenitor character through balancing the expression of ELF5 and GATA3. Taken together, we demonstrated that C1orf106 is an important regulator for basal-like/luminal progenitors and targeting C1orf106 is of therapeutic value for breast cancer.

Key words

C1orf106 basal-like luminal progenitor breast cancer ELF5 GATA3 

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Notes

Acknowledgements

This work was supported by the Ministry of Science and Technology of China (2016YFC1302103 and 2015CB553906), the National Natural Science Foundation of China (81230051, 81472734, 31170711, 81321003, and 30830048), the Beijing Natural Science Foundation (7120002), the 111 Project of the Ministry of Education, Peking University (BMU2018JC004, BMU20120314, and BMU20130364), and a Leading Academic Discipline Project of Beijing Education Bureau to H.Z. This work was also supported by a grant from the National Natural Science Foundation of China (81773199) to J.Z.

Compliance and ethics The author(s) declare that they have no conflict of interest.

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Copyright information

© Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature 2019

Authors and Affiliations

  • Ji Ma
    • 1
  • Cheng Liu
    • 1
  • Decao Yang
    • 1
  • Jiagui Song
    • 1
  • Jing Zhang
    • 1
  • Tianzhuo Wang
    • 1
  • Mengyuan Wang
    • 1
  • Weizhi Xu
    • 1
  • Xueying Li
    • 1
  • Shigang Ding
    • 2
    Email author
  • Jun Zhan
    • 1
    Email author
  • Hongquan Zhang
    • 1
    Email author
  1. 1.Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Anatomy, Histology and Embryology, and State Key Laboratory of Natural and Biomimetic DrugsPeking University Health Science CenterBeijingChina
  2. 2.Department of GastroenterologyPeking University Third HospitalBeijingChina

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