# LS174T
**LS174T** (also written LS 174T; full designation Laboratory of Surgery 174T) is a human colorectal adenocarcinoma cell line established in 1976 from the colon tumor of a 58-year-old woman with Dukes' type B disease, and used widely as a mucus-secreting, goblet-cell-like model of colon cancer[1](https://www.atcc.org/products/cl-188) • [2](https://www.cellosaurus.org/CVCL_1384). It is cataloged by the American Type Culture Collection as CL-188 and by ECACC as 87060401[1](https://www.atcc.org/products/cl-188) • [3](https://www.culturecollections.org.uk/nop/product/ls174t).
| Key fact | Detail |
|---|---|
| Origin | Established from a Dukes' type B adenocarcinoma of the colon; tissue minced and cultured without transfer for 10 months before line derivation[1](https://www.atcc.org/products/cl-188) |
| Donor | 58-year-old white female[1](https://www.atcc.org/products/cl-188) |
| Relationship to LS180 | Trypsin-dispersed variant of LS 180 (ATCC CL-187), derived from the same primary tumor; more easily subcultivated than the parent line[1](https://www.atcc.org/products/cl-188) |
| Secretory phenotype | Goblet cell type, mucus secreting; abundant microvilli and intracytoplasmic mucin vacuoles; produces large amounts of carcinoembryonic antigen (CEA)[1](https://www.atcc.org/products/cl-188) |
| Genomic status | Microsatellite instable (MSI); KRAS p.Gly12Asp (heterozygous), PIK3CA p.His1047Arg, CTNNB1 p.Ser45Phe (homozygous), no TP53 mutation reported[2](https://www.cellosaurus.org/CVCL_1384) |
| Tumorigenicity | Tumors developed within 21 days at 100% frequency (5/5) in nude mice inoculated subcutaneously with 107 cells[1](https://www.atcc.org/products/cl-188) |
| Growth | Adherent, epithelial morphology; reported population doubling times of 18 to 40 hours depending on study and passage[1](https://www.atcc.org/products/cl-188) • [2](https://www.cellosaurus.org/CVCL_1384) |
| Authentication caveat | Listed in the ICLAC Register of Misidentified Cell Lines as "LS-174T (LS-180 derivative)"[4](https://iclac.org/wp-content/uploads/Cross-Contaminations-v8_0.pdf) |
## Origin and relationship to LS180
The line was established by Baldwin H. Tom and colleagues at [Northwestern University](https://www.edgepedia.org/northwestern-university) and described in 1976 in *In Vitro* as "Human colonic adenocarcinoma cells. I. Establishment and description of a new line"[1](https://www.atcc.org/products/cl-188) • [2](https://www.cellosaurus.org/CVCL_1384). Two lines were derived from the same primary tumor by different subculture methods: the scraped culture was designated LS180, and the trypsin-dispersed culture LS174T[5](https://aacrjournals.org/cancerres/article/40/5/1443/484709/Longitudinal-Karyotype-and-Genetic-Signature). [Karyotype analysis](https://www.edgepedia.org/karyotype-analysis) during serial subcultivation showed that early LS174T passages consisted mainly of 46,XX (38%) and 45,X (34%) cells, with the 45,X karyotype predominating later; genetic signature analysis confirmed the common origin of the two lines, and the patient's normal bowel mucosa and blood leukocytes had normal 46,XX karyotypes[5](https://aacrjournals.org/cancerres/article/40/5/1443/484709/Longitudinal-Karyotype-and-Genetic-Signature). The ATCC karyotype entry for the distributed line reads 45,X, with one [X chromosome](https://www.edgepedia.org/x-chromosome) missing and no other chromosomal aberrations[1](https://www.atcc.org/products/cl-188).
Because LS174T is a derivative of LS180 rather than an independent isolation, it appears in the ICLAC Register of Misidentified Cell Lines under the entry "LS-174T (LS-180 derivative)"[4](https://iclac.org/wp-content/uploads/Cross-Contaminations-v8_0.pdf). The listing reflects the derivative relationship, not HeLa contamination; a 1977 survey found no HeLa contamination in the line[2](https://www.cellosaurus.org/CVCL_1384).
## Molecular characteristics
LS174T is microsatellite instable (MSI), a status documented across multiple independent studies[2](https://www.cellosaurus.org/CVCL_1384). Its recurrent driver mutations include KRAS p.Gly12Asp (heterozygous), PIK3CA p.His1047Arg, and a homozygous CTNNB1 p.Ser45Phe mutation in the beta-catenin destruction region; no TP53 mutation is reported, and the line is described as expressing wild-type TP53[2](https://www.cellosaurus.org/CVCL_1384) • [6](https://pmc.ncbi.nlm.nih.gov/articles/PMC8167241/). Earlier oncogene-expression profiling found expression of c-myc, N-myc, H-ras, N-ras, Myb, and fos, while K-ras and sis expression were not detected[1](https://www.atcc.org/products/cl-188).
The line expresses carcinoembryonic antigen, interleukin 6, interleukin 10, and mucin, and stains positively for cytokeratins[1](https://www.atcc.org/products/cl-188). Its HLA class I typing has been reported as HLA-A*02 with HLA-B*13 and B*50 in the ATCC record, with other studies reporting additional alleles[1](https://www.atcc.org/products/cl-188) • [2](https://www.cellosaurus.org/CVCL_1384).
## Divergence from LS180
Although the two lines share a tumor of origin, they have drifted apart in culture. A genomic comparison of paired colorectal cancer cell lines found 480 mutational differences between LS174T and LS180, with 0.4% of the genome differing in copy number; the pair is microsatellite-instable, where such divergence is larger than in nonhypermutated pairs[7](https://aacrjournals.org/cancerres/article-split/74/12/3238/592704/Colorectal-Cancer-Cell-Lines-Are-Representative). The same study notes that LS174T and LS180 differ in E-cadherin expression and cell adhesion, with LS174T showing complete loss of E-cadherin protein[7](https://aacrjournals.org/cancerres/article-split/74/12/3238/592704/Colorectal-Cancer-Cell-Lines-Are-Representative). Across the paired lines studied, mutation differences did not obscure known driver genes: 29 of 33 (87.9%) nonsilent mutations in established colorectal cancer genes were concordant between pairs[7](https://aacrjournals.org/cancerres/article-split/74/12/3238/592704/Colorectal-Cancer-Cell-Lines-Are-Representative).
## Use as a mucus and mucin model
LS174T functions as a secreting goblet cell model and is used in gastrointestinal barrier research to investigate mucus regulation in the gut and its role in drug permeation[1](https://www.atcc.org/products/cl-188). A quantitative comparison of MUC2 and MUC5AC mRNA across four colon cancer cell lines ranked MUC2 abundance LS174T > LoVo > HT-29 > Caco-2, making LS174T the highest MUC2 expresser of the four, while Caco-2 ranked highest for MUC5AC[8](https://www.sciencedirect.com/science/article/abs/pii/S0040816611000437). In that study LS174T cells also showed significantly higher proliferative and invasive capacities than Caco-2 cells[8](https://www.sciencedirect.com/science/article/abs/pii/S0040816611000437). Mucin-high variants of the line, such as the HM7 subline selected for high mucin production, have been used to study the link between mucin production and metastatic behavior[9](https://pmc.ncbi.nlm.nih.gov/articles/PMC2363198/).
## In vivo and drug-response behavior
LS174T is tumorigenic: subcutaneous inoculation of 107 cells into nude mice produced tumors in all five animals within 21 days[1](https://www.atcc.org/products/cl-188). In a large xenograft survey of 84 colorectal cancer cell lines grown in immunocompromised Balb/c nu/nu mice, LS174T was among the fastest-growing lines, with a tumor doubling time under 1 day, compared with more than 25 days for the slowest lines[10](https://pmc.ncbi.nlm.nih.gov/articles/PMC12141688/). Its MSI status is consistent with the faster growth observed for MSI versus microsatellite-stable tumors in that panel (median doubling time 3.7 versus 5.8 days)[10](https://pmc.ncbi.nlm.nih.gov/articles/PMC12141688/).
Because it carries a KRASG12D mutation, LS174T is a standard model for mutant-KRAS studies. The KRASG12D-selective inhibitor MRTX1133 selectively inhibits the growth of LS174T cells while being ineffective against lines lacking that mutation[11](https://www.nature.com/articles/s41698-026-01384-3). In KRAS-silencing experiments, LS174T cells were classified as resistant to KRAS silencing, whereas [SW480](https://www.edgepedia.org/sw480) cells were sensitive, and the G0 arrest signature induced by KRAS knockdown was weaker in LS174T than in HCT116 or SW480[12](https://pmc.ncbi.nlm.nih.gov/articles/PMC10896403/). In oxaliplatin sensitivity assays, LS174T was among the most sensitive lines in both monolayer (IC50 0.11) and spheroid (IC50 0.18) formats[13](https://pmc.ncbi.nlm.nih.gov/articles/PMC10452405/).
## Culture and handling
The line grows as an adherent epithelial monolayer in islands, with cells tending to pile up; ECACC advises splitting at roughly 40 to 50% confluence, seeding at 2 to 5 × 10,000 cells/cm² with 0.05% trypsin or trypsin/EDTA[3](https://www.culturecollections.org.uk/nop/product/ls174t). ATCC recommends Eagle's Minimum Essential Medium with 10% fetal bovine serum at 37 °C in 5% CO₂, with a subcultivation ratio of 1:2 to 1:4 and medium renewal two to three times per week[1](https://www.atcc.org/products/cl-188). Reported population doubling times vary with passage and laboratory: 26 hours at the 20th passage in the original description, 18 to 20 hours in a later study, 38.01 hours in another, and approximately 30 to 40 hours per DSMZ[2](https://www.cellosaurus.org/CVCL_1384). The line is distributed by multiple collections under accession numbers including ATCC CL-188, DSMZ ACC-759, and ECACC 87060401, and is cited in publications as LS174T (RRID:CVCL_1384)[2](https://www.cellosaurus.org/CVCL_1384) • [3](https://www.culturecollections.org.uk/nop/product/ls174t).
## References
1. [LS 174T (CL-188), ATCC product page](https://www.atcc.org/products/cl-188)
2. [Cellosaurus cell line LS174T (CVCL_1384)](https://www.cellosaurus.org/CVCL_1384)
3. [LS174T, Culture Collections (ECACC 87060401)](https://www.culturecollections.org.uk/nop/product/ls174t)
4. [Database of Cross-Contaminated or Misidentified Cell Lines, ICLAC (v8.0)](https://iclac.org/wp-content/uploads/Cross-Contaminations-v8_0.pdf)
5. [Rutzky LP, et al. (1980). Longitudinal Karyotype and Genetic Signature Analysis of Cultured Human Colon Adenocarcinoma Cell Lines LS180 and LS174T. Cancer Research 40:1443-1448](https://aacrjournals.org/cancerres/article/40/5/1443/484709/Longitudinal-Karyotype-and-Genetic-Signature)
6. [Influence of chronic inflammation on the malignant phenotypes and the plasticity of colorectal cancer cells (PMC8167241)](https://pmc.ncbi.nlm.nih.gov/articles/PMC8167241/)
7. [Colorectal Cancer Cell Lines Are Representative Models of the Main Molecular Subtypes of Primary Cancer. Cancer Research 74:3238 (2014)](https://aacrjournals.org/cancerres/article-split/74/12/3238/592704/Colorectal-Cancer-Cell-Lines-Are-Representative)
8. [Bu XD, et al. (2011). Caco-2 and LS174T cell lines provide different models for studying mucin expression in colon cancer. Tissue and Cell 43:201-206](https://www.sciencedirect.com/science/article/abs/pii/S0040816611000437)
9. [Butyrate regulates E-cadherin transcription, isoform expression and intracellular position in colon cancer cells (PMC2363198)](https://pmc.ncbi.nlm.nih.gov/articles/PMC2363198/)
10. [Model systems and unique biological features of high and low-grade colorectal cancer revealed by xenografting 84 human CRC cell lines (PMC12141688)](https://pmc.ncbi.nlm.nih.gov/articles/PMC12141688/)
11. [High-throughput screening identifies NT-1 that synergizes with MRTX1133 against acquired resistant KRASG12D colorectal cancer. npj Precision Oncology](https://www.nature.com/articles/s41698-026-01384-3)
12. [KRAS silencing alters chromatin physical organization and transcriptional activity in colorectal cancer cells (PMC10896403)](https://pmc.ncbi.nlm.nih.gov/articles/PMC10896403/)
13. [Luciferase Expressing Preclinical Model Systems Representing the Different Molecular Subtypes of Colorectal Cancer (PMC10452405)](https://pmc.ncbi.nlm.nih.gov/articles/PMC10452405/)
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*Topic: Encyclopedia › Life and health › Biological foundations › Cell biology › Cell culture methods › Colorectal cancer cell lines*
*Initially written Oct 21, 2026*
*Copyright 2026 EdgeChat AI, a subsidiary of Biostate AI.*
License: Edgepedia Community License 1.0, https://www.edgepedia.org/edgepedia/license