RKO
Cat.No.: CSC-C9242W
Species: Homo sapiens (Human)
Source: Intestine; Colon
Morphology: epithelial
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RKO is a line of human colorectal carcinoma cells. Established by Michael Brattain et al. from a primary colon carcinoma, RKO cells behave like most cancer cells morphologically (they are epithelial-like) and will grow aggressively in vitro as well as in xenograft assays. However, what sets RKO apart from other cancer cell lines is that it has well-defined mutations and epigenetic alterations. RKO is a microsatellite unstable (MSI-H) cell line due to epigenetic silencing of MLH1 via promoter hypermethylation. Therefore, RKO can be used as a model to study the "CIMP" pathway. Additionally, RKO has the BRAF (V600E) mutation and retains wild-type p53 expression, making it valuable for studying how oncogenic signaling interacts with wildtype tumor suppressor signaling. For this reason, it has become a popular cell line for performing high-throughput drug screens as well as DNA repair and gene editing studies because of its well-defined and understood behavior and sequenced genome.
EVs Isolated from Cur-Medium Inhibited RKO Cell Proliferation
Curcumin (Cur) is a natural phytochemical that is expected to become an indispensable drug for the treatment of colorectal cancer. A comprehensive understanding of the anti-tumor mechanism of Cur will provide a better reference for its clinical application. Xu's team aimed to examine the effects of extracellular vesicles (EVs) isolated from Cur-medium on RKO colorectal cancer cell proliferation, apoptosis, and migration.
RKO cells treated with 1.25-20 µM curcumin (Cur) for 48 hours showed survival rates of 91.23%±4.13% to 39.64%±3.26% (Fig. 1A), indicating dose-dependent viability reduction. They selected 1.25 µM and 10 µM Cur for further study. EVs were isolated from RKO cells treated with 1.25 µM and 10 µM Cur (Cur1-RKOEVs and Cur10-RKOEVs) (Fig. 1B). PKH67-labeled EVs were taken up by RKO cells (Fig. 1C). At 50 µg/mL, Cur1-RKOEVs and Cur10-RKOEVs had minimal impact on RKO cell survival (100.13%±1.48% and 97.07%±1.28%) or PCNA expression (Fig. 2, 3). However, at 100 µg/mL, Cur10-RKOEVs significantly reduced survival to 81.76%±1.84% and inhibited PCNA expression, while Cur1-RKOEVs had no significant effect (98.85%±1.51%) (Fig. 2, 3). This suggests that high-dose Cur-derived EVs inhibit RKO cell proliferation.
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