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Updated: Sep 30, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
Inverse GAS5-SFXN1 Correlation in Triple-Negative Breast Cancer: Insights from Bioinformatics and Tissue Expression
Pourya Sam Daliri1,2, Maryam Valizadeh-Otaghsara3, Mahdi Paryan4
1Hearing Disorders Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background:
Triple-negative breast cancer (TNBC) is an aggressive subtype with limited therapeutic options. Given the involvement of long non-coding RNAs, like GAS5, in cancer progression, this study aimed to identify GAS5-associated target genes through breast cancer databases and evaluate the expression levels of GAS5 and SFXN1 (as a potential target) in TNBC tissues.
Methods:
After predicting putative GAS5 targets via StarBase, they were validated through TCGA and GEPIA2. RT-qPCR was then performed to examine GAS5 and SFXN1 expression in 18 tumor and 15 adjacent normal samples. Gene expression levels were quantified using the fold-change method, and statistical analyses were performed using linear mixed models, one-sample t-tests, and Spearman's correlation.
Results:
Bioinformatics analyses revealed significant differential expression of SFXN1 in the TCGA and GEPIA2 databases. In the experimental validation phase, the mean Log2FC values for GAS5 and SFXN1 in tumor samples were 0.235 and -0.450, respectively. Neither gene showed a statistically significant difference between tumor and normal tissues using the t-test (GAS5: p = 0.650; SFXN1: p = 0.458). The linear mixed model also revealed no significant difference for either gene in the same comparison. Spearman's correlation, however, demonstrated a significant negative correlation between GAS5 and SFXN1 expression (r = -0.479; p = 0.049).
Conclusion:
While GAS5 and SFXN1 were not differentially expressed in TNBC tissues, their significant inverse correlation suggests a potential association that may contribute to the molecular networks underlying TNBC pathogenesis. Further functional studies are warranted to clarify this relationship. Any diagnostic or therapeutic implications remain speculative at this stage.
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