Tino Alexandria B, Dachs Gabi U, Sykes Peter H, Chitcholtan Kenny
Gynaecological Cancer Research Group, Department of Obstetrics and Gynaecology, University of Otago Christchurch, Christchurch, New Zealand.
Mackenzie Cancer Research Group, Department of Pathology and Biomedical Science, University of Otago Christchurch, Christchurch, New Zealand.
J Obstet Gynaecol Res. 2025 Aug;51(8):e70026. doi: 10.1111/jog.70026.
Advanced ovarian cancer involves tumor cells proliferating within ascitic fluid, which is rich in chemokines, cytokines, growth factors, and phospholipids essential for tumor progression. Tumor necrosis factor-alpha (TNF-α) and lysophosphatidic acid (LPA) are critical components that modulate ovarian tumor cell behavior in vivo, though most in vitro studies have relied on cell monolayers that do not accurately represent the tumor microenvironment. We thus investigated TNF-α and LPA effects on ovarian tumor cells cultured in collagen scaffolds, which are a model more reflective of in vivo conditions.
Ovarian cancer cell lines SKOV-3, OVCAR-8, OVCAR-5, and OVCAR-4 were cultured in collagen I hydrogels at various concentrations of TNF-α and LPA for 2-8 days. Outcomes included cell morphology, collagen topography, secretion of vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), interleukin-6 (IL-6), and cell survival endpoints, with comparisons to collagen topography observed in ovarian tumor tissue.
Collagen I fiber topography in 3D hydrogels remodeled over time, resembling the ovarian cancer tissue. LPA significantly reduced hydrogel size in SKOV-3 cells. While LPA modestly altered VEGF secretion, both LPA and TNF-α increased IL-8 secretion over time, with TNF-α also elevating IL-6 levels. TNF-α reduced cell survival in OVCAR-8 and OVCAR-5, while LPA promoted cell growth in SKOV-3, OVCAR-8, and OVCAR-5.
TNF-α and LPA have diverse, cell line-specific effects on ovarian cancer cells in collagen hydrogels, underscoring cell line heterogeneity and the utility of 3D models.
晚期卵巢癌涉及肿瘤细胞在富含趋化因子、细胞因子、生长因子和对肿瘤进展至关重要的磷脂的腹水中增殖。肿瘤坏死因子-α(TNF-α)和溶血磷脂酸(LPA)是在体内调节卵巢肿瘤细胞行为的关键成分,尽管大多数体外研究依赖于不能准确代表肿瘤微环境的细胞单层。因此,我们研究了TNF-α和LPA对在胶原支架中培养的卵巢肿瘤细胞的影响,胶原支架是一种更能反映体内情况的模型。
将卵巢癌细胞系SKOV-3、OVCAR-8、OVCAR-5和OVCAR-4在不同浓度的TNF-α和LPA的I型胶原水凝胶中培养2-8天。观察指标包括细胞形态、胶原形貌、血管内皮生长因子(VEGF)、白细胞介素-8(IL-8)、白细胞介素-6(IL-6)的分泌以及细胞存活终点,并与卵巢肿瘤组织中观察到的胶原形貌进行比较。
3D水凝胶中的I型胶原纤维形貌随时间重塑,类似于卵巢癌组织。LPA显著减小了SKOV-3细胞中的水凝胶大小。虽然LPA适度改变了VEGF的分泌,但随着时间的推移,LPA和TNF-α均增加了IL-8的分泌,TNF-α还提高了IL-6水平。TNF-α降低了OVCAR-8和OVCAR-5中的细胞存活率,而LPA促进了SKOV-3、OVCAR-8和OVCAR-5中的细胞生长。
TNF-α和LPA对胶原水凝胶中的卵巢癌细胞具有多种细胞系特异性作用,突出了细胞系的异质性和三维模型的实用性。