Yagel S, Parhar R S, Jeffrey J J, Lala P K
Department of Anatomy, University of Western Ontario, London, Canada.
J Cell Physiol. 1988 Sep;136(3):455-62. doi: 10.1002/jcp.1041360309.
First-trimester normal human trophoblast cells show some phenotypic similarities to malignant cells, e.g., rapid proliferation and ability to invade neighboring tissue, including basement membrane in situ, but do not have the ability for unlimited growth or metastasis. The present study examined whether the invasive ability of normal trophoblast cells is an intrinsic property of these cells, independent of the microenvironment provided by the pregnant uterus, and if so, whether they share some of the molecular mechanisms of invasion exercized by metastatic malignant cells. The ability of in vitro grown human trophoblast lines to invade an epithelium-free human amniotic membrane was measured from the temporal kinetics of retention of radioactivity within this membrane resulting from a penetration by 125I-iododeoxyuridine-labeled trophoblast cells. The magnitude of this invasion was compared to that of the highly metastatic human JAR-choriocarcinoma cell line and murine B16F10 melanoma line. Trophoblasts were found to share some of the same molecular mechanisms of invasion with the metastatic cell lines. Inhibitors of collagenase, plasmin, plasminogen, and plasminogen activators completely prevented invasion of the amnion by the trophoblast lines as well as by the metastatic JAR and B16F10 lines. Mersalyl, a compound known to activate collagenase, stimulated invasion by all cell lines tested, including under conditions in which plasmin activity was inhibited. In addition, trophoblasts produced significant levels of type IV collagenase and laminin, both of which appear to be important products of metastatic tumor cells required for basement membrane invasion. It may be concluded from these findings that the invasive property of first trimester human trophoblasts is genetically determined; that the magnitude of amnion invasion cannot differentiate between metastatic cell lines and invasive but nonmetastatic cell lines; and that invasiveness is not a sufficient prerequisite for metastatic ability.
妊娠早期正常人类滋养层细胞表现出与恶性细胞的一些表型相似性,例如快速增殖以及侵入邻近组织(包括原位基底膜)的能力,但不具备无限生长或转移的能力。本研究探讨正常滋养层细胞的侵袭能力是否是这些细胞的固有特性,独立于妊娠子宫提供的微环境,如果是这样,它们是否共享转移性恶性细胞行使的一些侵袭分子机制。通过125I - 碘脱氧尿苷标记的滋养层细胞穿透导致放射性在无上皮人羊膜内保留的时间动力学,测量体外培养的人滋养层细胞系侵入无上皮人羊膜的能力。将这种侵袭程度与高转移性人JAR - 绒毛膜癌细胞系和小鼠B16F10黑色素瘤细胞系的侵袭程度进行比较。发现滋养层细胞与转移性细胞系共享一些相同的侵袭分子机制。胶原酶、纤溶酶、纤溶酶原和纤溶酶原激活剂的抑制剂完全阻止了滋养层细胞系以及转移性JAR和B16F10细胞系对羊膜的侵袭。已知能激活胶原酶的化合物汞撒利刺激了所有测试细胞系的侵袭,包括在纤溶酶活性被抑制的条件下。此外,滋养层细胞产生大量的IV型胶原酶和层粘连蛋白,这两者似乎都是基底膜侵袭所需的转移性肿瘤细胞的重要产物。从这些发现可以得出结论,妊娠早期人类滋养层细胞的侵袭特性是由基因决定的;羊膜侵袭程度无法区分转移性细胞系和侵袭性但非转移性细胞系;并且侵袭性不是转移能力的充分先决条件。