Mikuła-Pietrasik Justyna, Uruski Paweł, Sosińska Patrycja, Maksin Konstantin, Piotrowska-Kempisty Hanna, Kucińska Małgorzata, Murias Marek, Szubert Sebastian, Woźniak Aldona, Szpurek Dariusz, Sajdak Stefan, Piwocka Katarzyna, Tykarski Andrzej, Książek Krzysztof
Department of Hypertensiology, Angiology and Internal Medicine, Poznań University of Medical Sciences, Długa 1/2 Str., Poznań 61-848, Poland.
Department of Pathophysiology; Poznań University of Medical Sciences, Rokietnicka 8 Str., Poznań 60-806, Poland.
Cell Death Dis. 2016 Dec 29;7(12):e2565. doi: 10.1038/cddis.2016.417.
Although both incidence and aggressiveness of ovarian malignancy rise with age, the exact reason for this tendency, in particular the contribution of senescent cells, remains elusive. In this project we found that the patient's age determines the frequency of intraperitoneal metastases of ovarian cancer. Moreover, we documented that senescent human peritoneal mesothelial cells (HPMCs) stimulate proliferation, migration and invasion of ovarian cancer cells in vitro, and that this effect is related to both the activity of soluble agents released to the environment by these cells and direct cell-cell contact. The panel of mediators of the pro-cancerous activity of senescent HPMCs appeared to be cancer cell line-specific. The growth of tumors in a mouse peritoneal cavity was intensified when the cancer cells were co-injected together with senescent HPMCs. This effect was reversible when the senescence of HPMCs was slowed down by the neutralization of p38 MAPK. The analysis of lesions excised from the peritoneum of patients with ovarian cancer showed the abundance of senescent HPMCs in close proximity to the cancerous tissue. Collectively, our findings indicate that senescent HPMCs which accumulate in the peritoneum in vivo may create a metastatic niche facilitating intraperitoneal expansion of ovarian malignancy.
尽管卵巢恶性肿瘤的发病率和侵袭性均随年龄增长而上升,但这种趋势的确切原因,尤其是衰老细胞的作用,仍不清楚。在本项目中,我们发现患者年龄决定了卵巢癌腹膜转移的频率。此外,我们证明衰老的人腹膜间皮细胞(HPMC)在体外可刺激卵巢癌细胞的增殖、迁移和侵袭,且这种作用与这些细胞释放到环境中的可溶性因子的活性以及细胞间直接接触均有关。衰老HPMC促癌活性的介质组似乎具有癌细胞系特异性。当癌细胞与衰老HPMC共同注射时,小鼠腹腔内肿瘤的生长加剧。当通过中和p38丝裂原活化蛋白激酶减缓HPMC的衰老时,这种作用是可逆的。对卵巢癌患者腹膜切除病变的分析显示,癌组织附近存在大量衰老HPMC。总体而言,我们的研究结果表明,体内积聚在腹膜中的衰老HPMC可能形成一个转移龛,促进卵巢恶性肿瘤的腹膜内扩展。