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[肿瘤细胞侵袭及侵袭能力增强与抑制的实验模型的建立]

[Establishment of an experimental model for tumor cell invasion and potentiation and inhibition of the invasive capacity].

作者信息

Akedo H, Shinkai K, Mukai M, Komatsu K

出版信息

Gan To Kagaku Ryoho. 1987 Jun;14(6 Pt 2):2048-55.

PMID:3606140
Abstract

Seeding of rat ascites hepatoma cells (AH 130) on cultured mesothelial cell monolayers resulted in the penetration of single tumor cells and subsequent formation of tumor cell colonies underneath the monolayers. Determination of the number of colonies facilitated quantitative estimation of the in vitro invasive ability, which corresponded well with the in vivo invasive capability of the tumor cells. Preculture of AH 130 cells with macrophages greatly potentiated both the in vitro and in vivo invasive capacities of the tumor cells. This potentiation seems to be mediated by certain species of active oxygen radicals generated by macrophages. Acid/ethanol extract of normal rat liver inhibited both the in vitro and in vivo invasion by the tumor cells. The inhibiting entity in the extract was heat-stable and had a molecular weight in the range of 3.5-10 Kd. It did not suppress tumor cell attachment to mesothelial cell layers, or inhibit tumor cell growth, but selectively impaired the penetration step of the tumor cell invasion through its binding to the tumor cell surface.

摘要

将大鼠腹水肝癌细胞(AH 130)接种于培养的间皮细胞单层上,导致单个肿瘤细胞穿透,并随后在单层下方形成肿瘤细胞集落。通过测定集落数量可对体外侵袭能力进行定量评估,这与肿瘤细胞的体内侵袭能力高度相符。将AH 130细胞与巨噬细胞预培养,可极大地增强肿瘤细胞的体外和体内侵袭能力。这种增强作用似乎是由巨噬细胞产生的某些活性氧自由基介导的。正常大鼠肝脏的酸/乙醇提取物可抑制肿瘤细胞的体外和体内侵袭。提取物中的抑制成分对热稳定,分子量在3.5 - 10千道尔顿范围内。它不抑制肿瘤细胞与间皮细胞层的附着,也不抑制肿瘤细胞生长,但通过与肿瘤细胞表面结合,选择性地损害肿瘤细胞侵袭的穿透步骤。

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