HT-29

Last updated September 02, 2022

HT-29 is a human colon cancer cell line used extensively in biological and cancer research.^[1]

Characteristics

The p53 protein, shown interacting with a strand of DNA, is overexpressed in HT-29 cells P53.png — The p53 protein, shown interacting with a strand of DNA, is overexpressed in HT-29 cells

Initially derived in 1964 by Jorgen Fogh from a 44-year-old Caucasian female, HT-29 cells form a tight monolayer while exhibiting similarity to enterocytes from the small intestine. HT-29 cells overproduce the p53 tumor antigen, but have a mutation in the p53 gene at position 273, resulting in a histidine replacing an arginine. The cells proliferate rapidly in media containing suramin, with corresponding high expression of the c-myc oncogene. However, c-myc is deregulated, but may have a relation with the growth factor requirements of HT-29 cells.^[2]

Applications

In preclinical research, HT-29 cells have been studied for their ability to differentiate and thus simulate real colon tissue in vitro, a characteristic that has made HT-29 useful for epithelial cell research.^[3] The cells can also be tested in vivo via xenografts with rodents. HT-29 cells terminally differentiate into enterocytes with the replacement of glucose by galactose in cell culture, and with the addition of butyrate or acids, the differentiation pathways can be closely studied along with their dependence on surrounding conditions.^[1] Accordingly, studies of HT-29 cells have shown induced differentation as a result of forskolin, Colchicine, nocodazole, and taxol,^[4] with galactose-mediated differentiation also causing the strengthening of adherens junctions.^[5]

Culturing

Though HT-29 cells can proliferate in cell culture lacking growth factors with a doubling time of around 4 days, the doubling time can be reduced to one day with added fetal bovine serum.^[2] The cells have high glucose consumption, and in standard medium containing 25 mM glucose and 10% serum, remain undifferentiated.^[1]

Related Research Articles

An oncogene is a gene that has the potential to cause cancer. In tumor cells, these genes are often mutated, or expressed at high levels.

In oncology, the Warburg effect is the observation that most cancer cells produce energy predominantly not through the 'usual' citric acid cycle and oxidative phosphorylation in the mitochondria as observed in normal cells, but through a less efficient process of 'aerobic glycolysis' consisting of high level of glucose uptake and glycolysis followed by lactic acid fermentation taking place in the cytosol, not the mitochondria, even in the presence of abundant oxygen. This observation was first published by Otto Heinrich Warburg, who was awarded the 1931 Nobel Prize in Physiology for his "discovery of the nature and mode of action of the respiratory enzyme". The precise mechanism and therapeutic implications of the Warburg effect, however, remain unclear.

Caco-2 is an immortalized cell line of human colorectal adenocarcinoma cells. It is primarily used as a model of the intestinal epithelial barrier. In culture, Caco-2 cells spontaneously differentiate into a heterogeneous mixture of intestinal epithelial cells. It was developed in 1977 by Jorgen Fogh at the Sloan-Kettering Institute for Cancer Research.

Cancer stem cells (CSCs) are cancer cells that possess characteristics associated with normal stem cells, specifically the ability to give rise to all cell types found in a particular cancer sample. CSCs are therefore tumorigenic (tumor-forming), perhaps in contrast to other non-tumorigenic cancer cells. CSCs may generate tumors through the stem cell processes of self-renewal and differentiation into multiple cell types. Such cells are hypothesized to persist in tumors as a distinct population and cause relapse and metastasis by giving rise to new tumors. Therefore, development of specific therapies targeted at CSCs holds hope for improvement of survival and quality of life of cancer patients, especially for patients with metastatic disease.

The study of the tumor metabolism, also known as tumor metabolome describes the different characteristic metabolic changes in tumor cells. The characteristic attributes of the tumor metabolome are high glycolytic enzyme activities, the expression of the pyruvate kinase isoenzyme type M2, increased channeling of glucose carbons into synthetic processes, such as nucleic acid, amino acid and phospholipid synthesis, a high rate of pyrimidine and purine de novo synthesis, a low ratio of Adenosine triphosphate and Guanosine triphosphate to Cytidine triphosphate and Uridine triphosphate, low Adenosine monophosphate levels, high glutaminolytic capacities, release of immunosuppressive substances and dependency on methionine.

Myc is a family of regulator genes and proto-oncogenes that code for transcription factors. The Myc family consists of three related human genes: c-myc (MYC), l-myc (MYCL), and n-myc (MYCN). c-myc was the first gene to be discovered in this family, due to homology with the viral gene v-myc.

<span class="mw-page-title-main">Peroxisome proliferator-activated receptor gamma</span> Protein-coding gene in the species Homo sapiens

Peroxisome proliferator- activated receptor gamma, also known as the glitazone reverse insulin resistance receptor, or NR1C3 is a type II nuclear receptor functioning as a transcription factor that in humans is encoded by the PPARG gene.

Protein NDRG1 is a protein that in humans is encoded by the NDRG1 gene.

Epithelial cell adhesion molecule (EpCAM) is a transmembrane glycoprotein mediating Ca²⁺-independent homotypic cell–cell adhesion in epithelia. EpCAM is also involved in cell signaling, migration, proliferation, and differentiation. Additionally, EpCAM has oncogenic potential via its capacity to upregulate c-myc, e-fabp, and cyclins A & E. Since EpCAM is expressed exclusively in epithelia and epithelial-derived neoplasms, EpCAM can be used as diagnostic marker for various cancers. It appears to play a role in tumorigenesis and metastasis of carcinomas, so it can also act as a potential prognostic marker and as a potential target for immunotherapeutic strategies.

Suppressor of tumorigenicity 14 protein, also known as matriptase, is a protein that in humans is encoded by the ST14 gene. ST14 orthologs have been identified in most mammals for which complete genome data are available.

Homeobox protein Hox-C6 is a protein that in humans is encoded by the HOXC6 gene. Hox-C6 expression is highest in the fallopian tube and ovary. HoxC6 has been highly expressed in many types of cancers including prostate, breast, and esophageal squamous cell cancer.

Protein CIP2A also known as cancerous inhibitor of PP2A (CIP2A) is a protein that in humans is encoded by the KIAA1524 gene.

Carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5) also known as CD66e, is a member of the carcinoembryonic antigen (CEA) gene family.

In molecular biology, mir-145 microRNA is a short RNA molecule that in humans is encoded by the MIR145 gene. MicroRNAs function to regulate the expression levels of other genes by several mechanisms.

In molecular biology miR-203 is a short non-coding RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms, such as translational repression and Argonaute-catalyzed messenger RNA cleavage. miR-203 has been identified as a skin-specific microRNA, and it forms an expression gradient that defines the boundary between proliferative epidermal basal progenitors and terminally differentiating suprabasal cells. It has also been found upregulated in psoriasis and differentially expressed in some types of cancer.

In molecular biology mir-22 microRNA is a short RNA molecule. MicroRNAs are an abundant class of molecules, approximately 22 nucleotides in length, which can post-transcriptionally regulate gene expression by binding to the 3' UTR of mRNAs expressed in a cell.

HCT116 is a human colon cancer cell line used in therapeutic research and drug screenings.

hPG80 refers to the extracellular and oncogenic version of progastrin. This name first appeared in a scientific publication in January 2020. Until that date, scientific publications only mention 'progastrin', without necessarily explicitly specifying whether it is intracellular or extracellular in the tumor pathological setting.

Oncometabolism is the field of study that focuses on the metabolic changes that occur in cells that make up the tumor microenvironment (TME) and accompany oncogenesis and tumor progression toward a neoplastic state.

References

1 2 3 Martínez-Maqueda, D; et al. (2015). "HT29 Cell Line". The Impact of Food Bioactives on Health. Springer. pp. 113–124. doi:10.1007/978-3-319-16104-4_11. ISBN 978-3-319-15791-7. PMID 29787047.
1 2 Coudray, Anne-Marie; et al. (1 December 1989). "Proliferation of the Human Colon Carcinoma Cell Line HT29: Autocrine Growth and Deregulated Expression of the c-myc Oncogene" (PDF). Cancer Research. 49 (23): 6566–6571. PMID 2684395.
↑ Hirn, M; et al. (1988). "HT-29 cells are an in vitro model for the generation of cell polarity in epithelia during embryonic differentiation". Proceedings of the National Academy of Sciences. 85 (1): 136–140. Bibcode:1988PNAS...85..136L. doi: 10.1073/pnas.85.1.136 . PMC 279498 . PMID 3277169.
↑ Cohen, E; et al. (August 1999). "Induced differentiation in HT29, a human colon adenocarcinoma cell line". Journal of Cell Science. 112 (16): 2657–2666. doi:10.1242/jcs.112.16.2657. PMID 10413674.
↑ Gout, S; et al. (1 October 2004). "Early enterocytic differentiation of HT-29 cells: biochemical changes and strength increases of adherens junctions". Experimental Cell Research. 299 (1): 498–510. doi:10.1016/j.yexcr.2004.06.008. PMID 15350547.

External links

Cellosaurus entry for HT-29

This cell biology article is a stub. You can help Wikipedia by expanding it.

This oncology article is a stub. You can help Wikipedia by expanding it.

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.

[one-1] 1 2 3 Martínez-Maqueda, D; et al. (2015). "HT29 Cell Line". The Impact of Food Bioactives on Health. Springer. pp. 113–124. doi:10.1007/978-3-319-16104-4_11. ISBN 978-3-319-15791-7. PMID 29787047.

[two-2] 1 2 Coudray, Anne-Marie; et al. (1 December 1989). "Proliferation of the Human Colon Carcinoma Cell Line HT29: Autocrine Growth and Deregulated Expression of the c-myc Oncogene" (PDF). Cancer Research. 49 (23): 6566–6571. PMID 2684395.

[3] Hirn, M; et al. (1988). "HT-29 cells are an in vitro model for the generation of cell polarity in epithelia during embryonic differentiation". Proceedings of the National Academy of Sciences. 85 (1): 136–140. Bibcode:1988PNAS...85..136L. doi: 10.1073/pnas.85.1.136 . PMC 279498 . PMID 3277169.

[4] Cohen, E; et al. (August 1999). "Induced differentiation in HT29, a human colon adenocarcinoma cell line". Journal of Cell Science. 112 (16): 2657–2666. doi:10.1242/jcs.112.16.2657. PMID 10413674.

[5] Gout, S; et al. (1 October 2004). "Early enterocytic differentiation of HT-29 cells: biochemical changes and strength increases of adherens junctions". Experimental Cell Research. 299 (1): 498–510. doi:10.1016/j.yexcr.2004.06.008. PMID 15350547.

[1]

[2]

[3]

[4]

[5]