Biopolym. Cell. 2026; 42(3):221-230.
https://doi.org/10.7124/bc.000BBC
Molecular Biomedicine
Characterization of S6K1 isoform mRNA expression in molecular subtypes of human breast tumors
1Kroupskaya I. V., 1Mazov A. V., 1Garifulin O. M., 1Kropyvko S. V., 3Syvak L. A., 4Verovkina N. O., 1Martsynyuk M. Ye., 2Demidov S. V., 1Filonenko V. V.
  1. Institute of Molecular Biology and Genetics, NAS of Ukraine
    150, Akademika Zabolotnoho Str., Kyiv, Ukraine, 03143
  2. Educational and Scientific Center "Institute of Biology and Medicine",
    Taras Shevchenko National University of Kyiv
    64/13, Volodymyrska Str., Kyiv, Ukraine, 01601
  3. State Institution «National Research Center for Radiation Medicine,
    Hematology and Oncology of the NAMS of Ukraine»
    119/121, Beresteiskyi Ave., Kyiv, Ukraine, 03115
  4. Brown University
    Providence RI 02906, USA

Abstract

Aim. To investigate the transcriptional profiles of RPS6KB1 mRNAs encoding canonical (p70/p85-S6K1) and novel (p60-S6K1) isoforms in clinical human breast tumor (BC) samples across major molecular subtypes (Luminal A, Luminal B (HER2+), and triple-negative (TNBC)) compared to adjacent histologically normal tissue. Methods. Total RNA was isolated from clinical breast tumors and paired adjacent tissues. Expression levels of ESR1, HER2, and specific S6K1 isoform transcripts were quantified using real-time qPCR. Statistical analysis was performed to evaluate relative gene expression and p70/p85-S6K1/p60-S6K1 transcript ratios. Results. Transcriptional profiling confirmed clinical subtyping and revealed distinct S6K1 isoform expression patterns. Canonical p70/p85-S6K1 transcript levels were markedly upregulated across all tumors, with the highest expression observed in HER2-positive Luminal B samples. Conversely, expression of the novel p60-S6K1 isoform was dramatically downregulated in all tumor types, with the lowest levels detected in TNBC. The p70/p85-S6K1/p60-S6K1 mRNA ratio was significantly altered in cancer tissues compared to normal counterparts. Conclusions. These findings corroborate the pro-oncogenic role of canonical S6K1 signaling and provide the first evidence that the p60-S6K1 isoform may exert tumor-suppressive functions.
Keywords: RPS6KB1, p85S6K1, p70S6K1, p60S6K1, breast cancer molecular subtypes, qPCR
Full text: (PDF, in English)

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