HCT 116 is an adherent cell line isolated from the colon of a patient with colon cancer. It has a mutation in codon 13 of the ras-proto-oncogene. This cell line is near-diploid and has a relatively stable genetic profile, making it a valuable in vitro model. This line can be utilized in cancer research and gastrointestinal (GI) research.

Understanding the roots and basic traits of HCT116 cells, such as their morphological features, genetic makeup, and cellular dimensions, is essential for researchers embarking on studies using this cell line.

Part of: NCI-60 cancer cell line panel. Population: Caucasian. Doubling time: 17.1 hours (PubMed= 22628656); 22 hours (PubMed= 23546019); 25.02 hours (PubMed= 25944804); 36 hours (PubMed= 25984343); 18.14 +- 0.051 hours (PubMed= 32927768); ~25-48 hours (DSMZ=ACC-581); 17.4 hours (NCI-DTP=HCT-116); ~21 hours (PBCF).

2008年6月15日 · HCT116 human colon cancer cell line in this in vivo model system provides a tool to dissect the molecular mechanism involved in the metastatic cascade. This orthotopic model of colon cancer fulfills the rate limiting steps of local invasion and distant colony formation in the process of metastases.

HCT116 (ATCC® CCL-247 ™) is a human colorectal carcinoma cell line initiated from an adult male. The cells are adherent with an epithelial morphology. Following implantation into immunocompromised mice, the cells form primary tumors and distant metastases.

2019年12月5日 · We investigated β-catenin localization, transcriptome, and phenotypic differences of HCT116 cells containing a wild-type (HCT116-WT) or mutant β-catenin allele (HCT116-MT), or parental cells...

Here, we report the building of two QSAR studies using molecular and NMR descriptors for the prediction of anticancer activity against the human colon carcinoma HCT116 cell line, using the value of half maximal inhibitory concentration (IC 50).

The HCT116 and NCM460 data for 24 h and 48 h were analyzed by two-way analysis of variance with cell type (HCT116 or NCM460), treatment concentration, and their interaction as fixed effects and experiment as a blocking factor.

HCT116 cells upregulated AKT, MAPK and PLC signaling under GFDS conditions to counter stress. In contrast, HCT116b cells downregulated these signaling molecules by dephosphorylating and thereby inactivating AKT, ERK and PLC gamma to induced cell death.

The HCT116 VIM RFP reporter cell line carries a knock-in red fluorescent protein (RFP) reporter, which was integrated before the stop codon at the last exon of the endogenous vimentin (VIM) gene. Epithelial to mesenchymal transition (EMT) has been recognized to play an important role in cancer cell metastasis and drug resistance.