While urine sample diffused from the well, specific anti-albumin antibody reacted in the agar forming a halo of precipitation around the well.
In contrast, all human EWS/FLI-1 and murine Ews/Fli-1-expressing clones grew efficiently in soft agar, forming large macroscopic colonies of greater than 200 cells, indicating anchorage-independent growth.
These cells were transformed, grew as anchorage-independent colonies in agar, and formed sarcoma-like tumours when injected subcutaneously into nude mice.
Moreover, the stimulation of these pathways coincides with the stage when the cells acquire the ability to grow in soft agar and form tumors in nude mice.
Taken together these results indicate that chronic CSE exposure induces the embryonic Wnt and Hh signaling pathways at the same time that the cells acquire the ability to grow in soft agar and form tumors in nude mice.
In attempts to study the mechanisms of nickel-induced carcinogenesis in human cells, an immortalized human osteoblastic cell line (HOS) that could not grow in soft agar or form tumors in athymic nude mouse was repeatedly treated with a water-soluble nickel compound (NiCl2) or a less water-soluble nickel compound crystalline (NiS).
They do not show adhesion-independent growth in soft agar but form capillary structures in Matrigel, a characteristic property of cultured endothelium.
Brain aggregates formed in agar base-coated 24-well dishes and were matured over 3 weeks.
In the presence of estrogen, both NEO and AS-4 were able to form colonies; however, there was a significant difference (P <0.01) in the ability to form colonies in agar between AS-4 (133 colonies) and the control clone (six colonies).
The cells grew easily in soft agar and formed tumours in athymic mice.
CSCs form colonies in agar, mammospheres in low-adherence cultures, and tumors following xenotransplantation in Scid mice.
