Treatment-Associated Regulation of Protease Serine 57 Gene Expression in Myeloid Leukaemia Cell Models

Kasap B., Sırma Ekmekci S., Emrence Z., Abacı N.

11. Multidisipliner Kanser Araştırma Kongresi , İstanbul, Türkiye, 2 - 05 Temmuz 2026, ss.1-10, (Özet Bildiri)

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: İstanbul
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.1-10
  • İstanbul Üniversitesi Adresli: Evet

Özet

Introduction and Aim: Protease serine 57 (PRSS57) is a serine protease-related gene with emerging relevance in haematopoiesis, yet its role in haematological malignancies remains undefined. This study aimed to evaluate treatment-associated PRSS57 expression changes in chronic and acute myeloid leukaemia models exposed to targeted or differentiation-inducing therapies.

Materials and Methods: K562 cell viability after imatinib, nilotinib, and dasatinib treatment was assessed by MTT assay at 24, 48, and 72 hours; IC₅₀ concentrations at 48 hours were selected for expression analyses. K562 cells were treated with these tyrosine kinase inhibitors, while THP-1, HL-60, and NB4 cells were treated with all-trans retinoic acid. Cells were collected at 24, 48, and 72 hours. PRSS57 expression was quantified by RT-qPCR using GAPDH or TBP as reference genes and the 2−ΔΔCt method. Complementary analyses included MYC, BCL2, and BAX expression in K562 cells and May–Grünwald–Giemsa staining in acute myeloid leukaemia cells.

Results: Tyrosine kinase inhibitors induced treatment- and time-dependent modulation of PRSS57 expression in K562 cells. Upregulation was most pronounced at 24 hours, particularly after nilotinib and dasatinib exposure, whereas expression tended to decline toward baseline at 72 hours. In acute myeloid leukaemia models, all-trans retinoic acid markedly increased PRSS57 expression in THP-1 cells, while HL-60 and NB4 cells showed minimal responses. MYC and BCL2 showed treatment-related alterations without a consistent BAX increase, and staining supported differentiation-associated morphological changes.

Discussion: PRSS57 appears dynamically and cell-line-specifically regulated after targeted or differentiation-associated stimulation. Its early induction after tyrosine kinase inhibitor exposure may reflect a transient transcriptional response to treatment-induced cellular stress and signalling reprogramming, rather than sustained cytotoxicity. The THP-1 response further suggests an association with differentiation-related cellular remodelling. PRSS57 may represent a treatment-responsive molecular marker; future functional studies should clarify whether its induction has an adaptive, protective, or apoptosis-related role in tyrosine kinase inhibitor-exposed cells.