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Updated: May 10, 2025

Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
Published on: October 2, 2020
SNORA47 affects stemness and chemotherapy sensitivity via EBF3/RPL11/c-Myc axis in luminal A breast cancer
Qilin Han1,2, Ying Zhou1, Zixian Dong1
1Department of Breast Surgery, the First Hospital of China Medical University, 155 Nanjing North Street, Heping District, Shenyang, Liaoning, 110001, China.
Abstract:
Chemotherapy sensitivity is an important factor that restricts the prognosis of breast cancer, and breast cancer stem cells (BCSCs) are the root cause of chemotherapy sensitivity. SNORA47, a member of the small nucleolar RNAs, has not been documented in the context of breast cancer, although it has been reported in lung cancer. In this study, high SNORA47 expression was linked to unfavorable survival outcomes among patients with Luminal A breast cancer in The Cancer Genome Atlas (TCGA). Among Luminal A patients, an elevated expression of SNORA47 correlated with high TNM stage (P = 0.049). SNORA47 was strongly associated with breast cancer stemness phenotype and tumor sensitivity in vivo and in vitro. Our findings demonstrated that SNORA47, through its interaction with early B-cell factor 3(EBF3), facilitated the translocation of ribosomal protein L11(RPL11), which as a modulator that subsequently regulates the expression levels of the oncogene c-Myc. These discoveries provided novel insights into the molecular mechanisms of breast cancer progression and suggested potential therapeutic targets for overcoming drug sensitivity by disrupting the SNORA47-EBF3-RPL11 axis.
Insights
High SNORA47 expression in Luminal A breast cancer is linked to poor survival and chemotherapy resistance. This small nucleolar RNA drives cancer stemness by regulating the c-Myc oncogene via the EBF3-RPL11 pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Chemotherapy resistance in breast cancer impacts patient prognosis.
- Breast cancer stem cells (BCSCs) are implicated in chemotherapy resistance.
- SNORA47, a small nucleolar RNA, is uncharacterized in breast cancer but known in lung cancer.
Purpose of the Study:
- To investigate the role of SNORA47 in breast cancer, particularly Luminal A subtype.
- To explore the association between SNORA47 expression and patient survival and tumor characteristics.
- To elucidate the molecular mechanism by which SNORA47 influences breast cancer stemness and drug sensitivity.
Main Methods:
- Analysis of SNORA47 expression in The Cancer Genome Atlas (TCGA) database for breast cancer patients.
- Correlation analysis of SNORA47 expression with clinical parameters like TNM stage.
- In vitro and in vivo experiments to assess the impact of SNORA47 on breast cancer stemness and tumor sensitivity.
- Investigation of molecular interactions involving SNORA47, EBF3, RPL11, and c-Myc.
Main Results:
- High SNORA47 expression correlated with unfavorable survival outcomes in Luminal A breast cancer patients.
- Elevated SNORA47 levels were associated with advanced TNM stage in Luminal A breast cancer.
- SNORA47 demonstrated a strong link to breast cancer stemness and tumor sensitivity both in vitro and in vivo.
- SNORA47 facilitates c-Myc regulation by interacting with EBF3 and influencing RPL11 translocation.
Conclusions:
- SNORA47 is a potential biomarker for poor prognosis in Luminal A breast cancer.
- The SNORA47-EBF3-RPL11 axis plays a critical role in regulating c-Myc and promoting breast cancer stemness.
- Targeting the SNORA47 pathway offers a potential therapeutic strategy to overcome chemotherapy resistance in breast cancer.
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