LS513 Cells

The LS513 cell line is a well-characterized colorectal carcinoma model derived from a primary tumor biopsy taken in 1985 from a 63-year-old Caucasian male patient. The tumor was classified as a Dukes’ C mucin-secreting cecal carcinoma located at the Bauhin valve. LS513 cells are adherent in nature and have demonstrated multidrug resistance (MDR), making them a valuable model for studying drug resistance mechanisms in colorectal cancer. These cells exhibit a 30% colony-forming efficiency in methylcellulose and are tumorigenic in nude mice, further validating their use in oncogenic studies.

At the genetic level, LS513 cells express several notable features. They are positive for the p53 wild-type oncogene and express carcinoembryonic antigen (CEA) on approximately 50% of the cells. Additionally, LS513 cells express major histocompatibility complex (MHC) class I antigens, including HLA and beta 2 microglobulin, but lack MHC class II antigens (HLA-DR, DQ, and DP). The cells also produce transforming growth factor beta 1 (TGF beta-1) at a rate of 83 pg per 106 cells per 24 hours. Notably, TGF beta-1 acts as an inhibitor of LS513 cell proliferation, whereas TGF beta-2 has no significant effect on their growth. Compared to the LS1034 cell line, LS513 cells are 100-fold less sensitive to TGF beta-1, indicating distinct responses to growth factor signaling between these two colorectal carcinoma models.

LS513 cells exhibit a unique profile of antigen expression, with strong positivity for intercellular adhesion molecule 1 (ICAM-1) and HLA class I antigens. The lack of MHC class II antigen expression is particularly noteworthy, as it suggests potential immune evasion mechanisms that could be relevant to colorectal cancer progression and metastasis. These features, along with their resistance to multiple drugs and their ability to form tumors in immunocompromised mice, make LS513 cells a powerful tool for studying the molecular and cellular underpinnings of colorectal cancer, especially in the context of immune interactions and therapeutic resistance.