دورية أكاديمية
Secondary Analysis of Human Bulk RNA-Seq Dataset Suggests Potential Mechanisms for Letrozole Resistance in Estrogen-Positive (ER+) Breast Cancer.
العنوان: | Secondary Analysis of Human Bulk RNA-Seq Dataset Suggests Potential Mechanisms for Letrozole Resistance in Estrogen-Positive (ER+) Breast Cancer. |
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المؤلفون: | Sutherland L; Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA., Lang J; Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA., Gonzalez-Juarbe N; J. Craig Venter Institute, Rockville, MD 20850, USA.; Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA., Pickett BE; Department of Microbiology and Molecular Biology, Brigham Young University, Provo, UT 84602, USA. |
المصدر: | Current issues in molecular biology [Curr Issues Mol Biol] 2024 Jul 06; Vol. 46 (7), pp. 7114-7133. Date of Electronic Publication: 2024 Jul 06. |
نوع المنشور: | Journal Article |
اللغة: | English |
بيانات الدورية: | Publisher: MDPI Country of Publication: Switzerland NLM ID: 100931761 Publication Model: Electronic Cited Medium: Internet ISSN: 1467-3045 (Electronic) Linking ISSN: 14673037 NLM ISO Abbreviation: Curr Issues Mol Biol Subsets: PubMed not MEDLINE |
أسماء مطبوعة: | Publication: 2021- : Basel, Switzerland : MDPI Original Publication: Wymondham, Norfolk, UK : Caister Academic Press, |
مستخلص: | Estrogen receptor-positive (ER+) breast cancer is common among postmenopausal women and is frequently treated with Letrozole, which inhibits aromatase from synthesizing estrogen from androgens. Decreased estrogen slows the growth of tumors and can be an effective treatment. The increase in Letrozole resistance poses a unique problem for patients. To better understand the underlying molecular mechanism(s) of Letrozole resistance, we reanalyzed transcriptomic data by comparing individuals who responded to Letrozole therapy (responders) to those who were resistant to treatment (non-responders). We identified SOX11 and S100A9 as two significant differentially expressed genes (DEGs) between these patient cohorts, with "PLK1 signaling events" being the most significant signaling pathway. We also identified PRDX4 and E2F8 gene products as being the top mechanistic transcriptional markers for ER+ treatment resistance. Many of the significant DEGs that we identified play a known role in ER+ breast cancer or other types of cancer, which partially validate our results. Several of the gene products we identified are novel in the context of ER+ breast cancer. Many of the genes that we identified warrant further research to elucidate the more specific molecular mechanisms of Letrozole resistance in this patient population and could potentially be used as prognostic markers with further wet lab validation. We anticipate that these findings could contribute to improved detection and therapeutic outcomes in aromatase-resistant ER+ breast cancer patients. |
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فهرسة مساهمة: | Keywords: breast cancer; estrogen receptor; letrozole; transcriptional mechanisms; treatment resistance |
تواريخ الأحداث: | Date Created: 20240726 Latest Revision: 20240728 |
رمز التحديث: | 20240728 |
مُعرف محوري في PubMed: | PMC11275280 |
DOI: | 10.3390/cimb46070424 |
PMID: | 39057065 |
قاعدة البيانات: | MEDLINE |
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