TP53 Knockout HCT 116 Cell Line

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TP53 Knockout HCT 116 Cell Line
Cat.No.:

EDC07854

Species:

Human

Cell Name:

HCT 116

Gene:

TP53

Gene ID:

7157

Size:

1×10⁶cells

TP53 Knockout Cell Line (HCT116) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC07854
Product Name TP53 Knockout Cell Line (HCT116)
Cell line HCT 116
Cellosaurus ID CVCL_0291
Cell Line Synonyms HCT-116, HCT.116, HCT_116, HCT116, HCT116wt, HCT-116/P, HCT-116/parental, CoCL2
Gene TP53
NCBI Gene ID
Gene Synonyms BCC7|BMFS5|LFS1|P53|TRP53
Summary
This gene encodes a tumor suppressor protein containing transcriptional activation, DNA binding, and oligomerization domains. The encoded protein responds to diverse cellular stresses to regulate expression of target genes, thereby inducing cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. Mutations in this gene are associated with a variety of human cancers, including hereditary cancers such as Li-Fraumeni syndrome. Alternative splicing of this gene and the use of alternate promoters result in multiple transcript variants and isoforms. Additional isoforms have also been shown to result from the use of alternate translation initiation codons from identical transcript variants (PMIDs: 12032546, 20937277). [provided by RefSeq, Dec 2016]
Associated Diseases Colorectal Carcinoma
Morphology Adherent
Passage Ratio 1/5-1/4，2days
Complete Culture Medium mcCoy5A+10%FBS
Freezing Medium 90%FBS/Complete culture medium +10% DMSO
QC Indels validated by Sanger sequencing; sterility confirmed via microbial testing.
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: HCT 116		STR Info (Cell bank)
Cell Line: HCT 116
Allele1Allele2Allele3Allele4Allele1Allele2Allele3Allele4
Amelogenin X X
CSF1PO 7 10 7 9 10 11
D2S1338 16 16
D3S1358 12 17 18 19 12 18 19
D5S818 10 11 10 11
D7S820 11 12 11 12
D8S1179 10 12 14 15 10 12 14 15
D13S317 10 12 10 12
D16S539 11 13 11 12 13 14
D18S51 16 17 16 17
D19S433 12 13 12
D21S11 29 30 29 30
FGA 18 23 18 23
Penta D 9 13 9 13
Penta E 12 13 14 12 13 14
TH01 8 9 8 9
TPOX 8 8
vWA 17 21 22 23 17 21 22 23
D6S1043 13
D12S391 17 21 22
D2S441 11 12
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.

FAQ

Primary applications: • p53 target gene analysis: comparison of basal and stress-induced gene expression between p53-WT HCT 116 and the EDITGENE knockout, particularly for canonical p53 targets (p21/CDKN1A, MDM2, PUMA, BAX). • Chemotherapy sensitivity: dose-response analysis for 5-FU, oxaliplatin, irinotecan, and MDM2 inhibitors — drugs whose efficacy is influenced by p53 status in colorectal cancer. • DNA damage response: γH2AX dynamics, cell cycle checkpoint integrity, and apoptosis kinetics following ionizing radiation or genotoxic stress in the p53-null background. • Cancer phenotype assays: proliferation, anchorage-independent growth, and tumorigenicity in xenograft models for studying p53 loss effects in a colorectal cancer context. EDITGENE recommends this model for researchers investigating p53 tumor suppressor biology, colorectal cancer mechanisms, and p53-status-dependent therapeutic response.
Yes. p53 rescue experiments in HCT 116 are well-established in cancer biology research: • Construct design: use a codon-modified TP53 sequence with a small C-terminal tag (FLAG, HA). The N-terminal transactivation domain is critical — avoid large N-terminal modifications. • Hotspot mutation rescue: cancer-associated p53 mutations (R175H, R248W, R273H, R282W) enable genotype-function correlation in a colorectal cancer-relevant background. R175H/R282W are conformational mutants; R248W/R273H are DNA-contact mutants — these classes have distinct downstream consequences. • Transactivation-dead rescue: the L22Q/W23S mutation abolishes p53 transcriptional activity and serves as a control for transcription-dependent versus transcription-independent functions. • Expression level: p53 levels are tightly regulated; overexpression triggers stress responses that confound interpretation. Use inducible (Tet-On) systems calibrated to endogenous levels. HCT 116 transduces efficiently with lentivirus; the MSI-high background should be considered when comparing with microsatellite-stable colorectal lines.
The choice depends on whether you are studying p53's tumor suppressor functions in colorectal cancer biology or using p53 status as a variable in drug response research. The Knockout line is the standard tool for both — HCT 116 has long served as a foundational cancer cell line for p53 research, with the parental p53 wild-type and derivative p53-null variants forming one of the most extensively cited isogenic pairs in cancer biology. Overexpression is useful for rescue experiments and for studying p53 hotspot mutations in a colorectal cancer-relevant background. For colorectal cancer p53 research, the EDITGENE TP53 Knockout in HCT 116 is a workhorse research tool — the parental line's MSI-high status and well-characterized oncogenic mutation profile (KRAS G13D, PIK3CA H1047R) create a defined cancer-genetic context for studying p53 loss. Rescue with wild-type or hotspot mutant (R175H, R248W, R273H, R282W) p53 enables genotype-function correlation studies particularly relevant to colorectal cancer.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

Related Publications

IF=2.6
PloS one
The p53 protein is crucial for regulating cell survival and apoptosis in response to DNA damage. However, its influence on therapy effectiveness is controversial: when DNA damage is high p53 directs cells toward apoptosis, while under moderate genotoxic stress it saves the cells from death and promote DNA repair. Furthermore, these processes are influenced by the metabolism of transition metals, particularly copper since they serve as cofactors for critical enzymes. The metallochaperone Atox1 is under intensive study in this context because it serves as transcription factor allegedly mediating described effects of copper. Investigating the interaction between p53 and Atox1 could provide insights into tumor cell survival and potential therapeutic applications in oncology. This study explores the relationship between p53 and Atox1 in HCT116 and A549 cell lines with wild type and knockout TP53. The study found an inverse correlation between Atox1 and p53 at the transcriptional and translational levels in response to genotoxic stress. Atox1 expression decreased with increased p53 activity, while cells with inactive p53 had significantly higher levels of Atox1. Suppression of both genes increased apoptosis, while suppression of the ATOX1 gene prevented apoptosis even under the treatment with chemotherapeutic drugs. The findings suggest that Atox1 may act as one of key elements in promotion of cell cycle under DNA-damaging conditions, while p53 works as an antagonist by inhibiting Atox1. Understanding of this relationship could help identify potential targets in cell signaling pathways to enhance the effectiveness of combined antitumor therapy, especially in tumors with mutant or inactive p53.

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