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Updated: Nov 29, 2025

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer
Published on: January 12, 2020
SNORA72 Activates the Notch1/c-Myc Pathway to Promote Stemness Transformation of Ovarian Cancer Cells
Liwen Zhang1,2,3,4, Rong Ma1,2,3,4, Mengcong Gao1,2,3,4
1Department of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.
Abstract:
Cancer stem cells (CSCs) are responsible for the migration and recurrence of cancer progression. Small nucleolar RNAs (snoRNAs) play important roles in tumor development. However, how snoRNAs contribute to the regulation of the stemness of ovarian CSCs (OCSCs) remains unclear. In the present study, we found that SNORA72 was significantly upregulated in OVCAR-3 spheroids (OS) and CAOV-3 spheroids (CS) with the OCSC characteristics attained by serum-free culture in a suspension of OVCAR-3 (OV) and CAOV-3 (CA) cells. The overexpression of SNORA72 increased self-renewal abilities and migration abilities in OV and CA cells and upregulated the expressions of the stemness markers Nanog, Oct4, and CD133. In addition, the ectopic expression of SNORA72 can elevate the messenger RNA (mRNA) and protein expression levels of Notch1 and c-Myc in parental cells. The opposite results were observed in SNORA72-silenced OCSCs. Moreover, we found that Notch1 knockdown inversed the migration abilities and self-renewal abilities raised by overexpressing SNORA72. In summary, stemness transformation of ovarian cancer cells can be activated by SNORA72 through the Notch1/c-Myc pathway. This study introduces a novel therapeutic strategy for improving the treatment efficiency of ovarian cancer.
Insights
Small nucleolar RNA SNORA72 promotes ovarian cancer stem cell properties, enhancing self-renewal and migration. This occurs via the Notch1/c-Myc pathway, offering a potential therapeutic target for ovarian cancer.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Cancer stem cells (CSCs) drive tumor progression, metastasis, and recurrence.
- Small nucleolar RNAs (snoRNAs) are implicated in various cancers, but their role in ovarian CSCs is largely unexplored.
Purpose of the Study:
- To investigate the function of SNORA72 in regulating the stemness of ovarian cancer stem cells (OCSCs).
- To elucidate the molecular mechanisms underlying SNORA72's effects on OCSCs.
Main Methods:
- Serum-free culture of OVCAR-3 and CAOV-3 cells to induce OCSC characteristics.
- Overexpression and silencing of SNORA72.
- Assessment of self-renewal and migration abilities.
- Analysis of stemness markers (Nanog, Oct4, CD133) and signaling pathway components (Notch1, c-Myc) via mRNA and protein expression.
- Notch1 knockdown experiments.
Main Results:
- SNORA72 was significantly upregulated in OCSCs.
- SNORA72 overexpression enhanced OCSC self-renewal, migration, and stemness markers.
- SNORA72 upregulated Notch1 and c-Myc expression.
- SNORA72 silencing reversed these effects.
- Notch1 knockdown counteracted the pro-stemness effects of SNORA72.
Conclusions:
- SNORA72 activates ovarian cancer cell stemness through the Notch1/c-Myc pathway.
- SNORA72 represents a novel therapeutic target for enhancing ovarian cancer treatment efficacy.
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