Galyamina M A, Pobeguts O V, Bogomiakova M E, Smirnov I P, Sikamov K V, Gorbachev A Y
Lopukhin Federal Research and Clinical Center of Physical-Chemical Medicine, Federal Medical-Biological Agency of Russia, Moscow, Russia.
Bull Exp Biol Med. 2025 Mar;178(5):637-642. doi: 10.1007/s10517-025-06389-9. Epub 2025 Apr 29.
Previously, a link between mycoplasmas and the development of malignant neoplasms, particularly prostate cancer, had been shown. However, the mechanisms responsible for the oncogenic properties of mycoplasmas remain poorly understood. We have developed an infectious model of LNCaP prostate lymph node carcinoma cell line infection with Mycoplasma hominis (MHO). It has been shown that MHO can easily attach and invade into cells without reducing the growth rate or affecting morphology of LNCaP cells. Proteomic analysis has shown that during infection, MHO undergoes a significant functional restructuring decelerating its growth and leading to formation of mini colonies. This reorganization is associated with a shift in energy metabolism a less energy-efficient nucleoside utilization pathway. To adapt within LNCaP, MHO changes its repertoire of membrane proteins, variable antigens involved in adhesion and protection from host immunity. It is hypothesized that the transcription factor YebC plays a role in MHO survival within the eukaryotic cell.
此前,已证实支原体与恶性肿瘤尤其是前列腺癌的发生发展之间存在联系。然而,支原体致癌特性的相关机制仍知之甚少。我们建立了人型支原体(MHO)感染LNCaP前列腺淋巴结癌细胞系的感染模型。结果表明,MHO能够轻易附着并侵入细胞,而不降低LNCaP细胞的生长速率或影响其形态。蛋白质组学分析表明,在感染过程中,MHO经历了显著的功能重组,减缓了其生长并导致微小菌落的形成。这种重组与能量代谢的转变相关,即核苷利用途径的能量效率降低。为了在LNCaP细胞内存活,MHO改变了其膜蛋白库,即参与黏附及抵御宿主免疫的可变抗原。据推测,转录因子YebC在MHO在真核细胞内的存活中发挥作用。