HCT-15

Cat.No.: CSC-C0410

Species: Homo sapiens (Human)

Source: Intestine; Colon

Morphology: epithelial

Culture Properties: Adherent

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  • Background
  • Scientific Data
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Cat.No.
CSC-C0410
Description
Established from a colorectal adenocarcinoma; HCT-15 is a sister cell line of the cell line DLD-1. The HCT-15 cells are CSAp negative (CSAp-). They are positive for keratin by immunoperoxidase staining.
Species
Homo sapiens (Human)
Source
Intestine; Colon
Recommended Medium
Culture Properties
Adherent
Morphology
epithelial
STR DNA Profile
Amelogenin: X,Y
CSF1PO: 12
D13S317: 8,11
D16S539: 12,13
D5S818: 13
D7S820: 10,12
THO1: 7,9.3
TPOX: 8,11
vWA: 18,19
Karyotype
Human pseudodiploid karyotype with 16% polyploidy - 46<2n>XYq+, t(8;17) (p23;q12/21), inv(11)(p14.2;q13) - stable karyotypic differences cf DLD-1 - matches published karyotype
Application
The HCT-15 cell line can be used for tumourigenicity studies and also can be used as a suitable transfection host.

Disease
Colon Adenocarcinoma
Quality Control
Mycoplasma: negative in DAPI, microbiological culture, RNA hybridization, PCR assays
Immunology: cytokeratin +, cytokeratin-7 -, cytokeratin-8 +, cytokeratin-17 -, cytokeratin-18 +, cytokeratin-19 +, desmin -, endothel -, EpCAM +, GFAP -, neurofilament -
Storage and Shipping
liquid nitrogen vapor phase
Synonyms
HCT 15; HCT.15; HCT15
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

HCT‑15 is a human colorectal adenocarcinoma cell line originally derived in the early 1970s from the primary colon tumor of a male patient with Dukes C disease. Morphologically, HCT‑15 cells grow in an epithelial‑like manner as an adherent monolayer with a cobblestone appearance. Clusters of floating cells are also found, which represents the cellular heterogeneity of solid tumors. On a cytogenetic level, HCT‑15 is hyperdiploid with multiple chromosomal aberrations. Most notably, it harbors the translocations t(8;17)(p23;q21) and inv(11)(p15.3;q13.1) as well as loss of chromosomes 8, 11 and 17. Molecularly, HCT‑15 has activating mutations in KRAS and loss‑of‑function alterations in TP53 that cause aggressive growth and intrinsic resistance to a variety of chemotherapeutic agents. It is carcinoembryonic antigen (CEA)-expressing (~5.4 ng per 10⁶ cells per 10 days), keratin-positive but CSAp-negative on immunocytochemical staining.

In vivo, the cell line readily forms tumors in nude mice with a 100 % take rate within three weeks and is thus a reliable xenograft model for sub‑cutaneous and orthotopic colon cancer studies. Its pronounced resistance to 5‑fluorouracil, SN‑38 (active metabolite of irinotecan) and taxanes has allowed for the creation of several drug‑resistant sub‑lines, e.g., HCT‑15/FU, that are widely used to study chemoresistance mechanisms.

Represents normal HCT-15 cell line.

Fig. 1. Represents normal HCT-15 cell line (Gautam N, Kaur M, et al., 2016).

Biogenic PR-Agnps Inhibit Cell Proliferation in Colon Cancer HCT-15 Cells

Biosynthesized nanoparticles show promise in improving chemotherapy effectiveness, but there is limited research on biogenic silver nanoparticles from terrestrial ferns. Datkhile et al. investigated the effects of silver nanoparticles synthesized from Pteridium revolutum on inhibiting proliferation and inducing apoptosis in HCT-15 cancer cells.

In vitro studies evaluated the inhibitory effects of biogenic PR-AgNPs on HCT-15 colon cancer cells. PR-AgNPs exhibited dose-dependent cytotoxicity (2.5-15.0 µg/mL), with cell viability decreasing as concentration increased (Fig. 1A). MTT assay results showed significant suppression of HCT-15 cell proliferation after 24 h, with IC50 and IC90 values of 5.79±0.58 µg/mL and 13.82±1.38 µg/mL, respectively. Complete growth inhibition was achieved at 15 µg/mL. Morphological changes, including cell shrinkage, were observed in HCT-15 cells treated with 10-15 µg/mL PR-AgNPs (Fig. 1B), contrasting with healthy control cells. PR-AgNPs induced intracellular suicide in HCT-15 cells, leading to compromised cell membrane integrity, cytoplasmic condensation, and apoptotic cell death. Normal fibroblast cells from breast cancer tissue exhibited low toxicity when exposed to PR-AgNPs. Even at 15 µg/mL, PR-AgNPs inhibited less than 40.70±11.83% of fibroblast cell growth after 24 h.

Representative histogram showing in vitro dose dependent cytotoxicity of biogenic PR-AgNPs on HCT-15 cells.

Fig. 1. Representative histogram showing in vitro dose dependent cytotoxicity of biogenic PR-AgNPs on HCT-15 cells (Datkhile K D, Durgawale P P, et al., 2024).

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