3rd International Conference on Chemo and BioInformatics, Kragujevac, September 25-26. 2025. (pp. 265-268)
АУТОР(И) / AUTHOR(S): Enes Mehmet Serbetci, Halime Akgun, Oguzhan Akgun, Huseyin Emirhan Onur, Didem Akyoney, Elif Erturk, Digdem Yoyen Ermis, Haluk Barbaros Oral, Ferda Ari
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DOI: 10.46793/ICCBIKG25.265S
САЖЕТАК / ABSTRACT:
Apoptosis is one of the fundamental mechanisms that prevents cancer development and has traditionally been regarded as irreversible once critical molecular events, such as caspase activation, have occurred. However, accumulating evidence has demonstrated that certain cells can survive even after entering advanced stages of apoptosis through a process known as anastasis. This phenomenon is thought to contribute to the development of therapeutic resistance and the emergence of more aggressive tumor phenotypes. Since cell fate decisions during and after anastasis are tightly regulated at the transcriptional level, and transcriptional control is largely governed by chromatin dynamics, investigating the associated epigenetic alterations provides critical insight into how these cells adapt and potentially acquire malignant traits.
In this study, apoptosis was induced in non-small cell lung cancer cells using paclitaxel, and the surviving cells were subsequently re-cultured under drug-free conditions ed by a decrease. Western blot analyses revealed a significant increase in H3K9 and H3K27 levels, accompani in HDAC1 and HDAC2 expression (p < 0.05). qPCR results further confirmed these findings and demonstrated a statistically significant concordance with the Western blot data. These results suggest that anastasis is not merely an escape from cell death but also initiates an adaptive process involving epigenetic regulatory mechanisms. Overall, our findings highlight that targeting chromatin-modifying enzymes during anastasis may represent a promising therapeutic strategy to reduce the risk of recurrence and progression of post-apoptotic tumor cells.
КЉУЧНЕ РЕЧИ / KEYWORDS:
anastasis, non-small cell lung cancer, epigenetic, histone modification
ПРОЈЕКАТ / ACKNOWLEDGEMENT:
This research was supported by the Scientific and Technological Research Council of Türkiye (TÜBİTAK, 1001 Project No. 123Z073). We thank Bursa Uludag Molecular Cancer Research Laboratory (BUMKAL) for their valuable support and contributions to this study.
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