hct116 (ATCC)
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hct116
Hct116, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4038 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hct116/product/ATCC
Average 99 stars, based on 4038 article reviews
Hct116, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4038 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/hct116/product/ATCC
Average 99 stars, based on 4038 article reviews
hct116 - by Bioz Stars,
2026-04
99/100 stars
Images
1) Product Images from "4-Acetylantrocamol LT3 suppresses colorectal cancer growth and metastasis via PI3K/AKT and MAPK pathway modulation"
Article Title: 4-Acetylantrocamol LT3 suppresses colorectal cancer growth and metastasis via PI3K/AKT and MAPK pathway modulation
Journal: International Journal of Molecular Medicine
doi: 10.3892/ijmm.2026.5797
Figure Legend Snippet: Effects of four Antrodia cinnamomea -derived triterpenoid compounds on CRC cell viability. Cell viability was assessed by Cell Counting Kit-8 assay in three human CRC cell lines: (A) HCT116 (KRAS mutant), (B) HT29 (KRAS wild-type) and (C) Caco-2 (KRAS wild-type) after treatment with increasing concentrations (0.1, 1, 3 and 10 μ M) of DeEA, DSA, 4AAQB and LT4 for 24, 48 and 72 h. Absorbance was recorded at 450/650 nm and normalized to vehicle-treated controls (0.1% DMSO). Data are presented as the mean ± SD from at least three independent experiments (n≥3). * P<0.05, ** P<0.01, *** P<0.001 vs. vehicle-treated control. CRC, colorectal cancer; DeEA, dehydroeburicoic acid; DSA, dehydrosulphurenic acid; 4AAQB, 4-acetylantroquinonol B; LT4, 4-acetylantrocamol LT3.
Techniques Used: Derivative Assay, Cell Counting, Mutagenesis, Control
Figure Legend Snippet: LT4 suppresses colony formation, cell migration and EMT in HCT116 cells. (A) Colony formation assay was performed after treating HCT116 cells with various concentrations of LT4 (0.1, 1, 3 and 10 μ M) for 14 days. Colonies were stained with crystal violet and quantification of colony growth was calculated relative to the vehicle-treated Ctrl. (B) Wound healing assay showing inhibition of cell migration by LT4 (0.1, 1, 3 and 10 μ M) at 24, 48 and 72 h post-scratch. Representative images and quantified healing rates are shown. Western blot analysis of EMT-related proteins (C) N-cadherin (140 kDa), (D) E-cadherin (130 kDa) and (E) Vimentin (54 kDa) in HCT116 cells after 24-h LT4 treatment (0.1, 1, 3 and 10 μ M). β-actin (45 kDa) served as the loading control. The corresponding bar graphs show semi-quantification of N-cadherin/β-actin, E-cadherin/β-actin and vimentin/β-actin expressed as fold change relative to the vehicle-treated Ctrl. Data are presented as the mean ± SD from three independent experiments (n=3). * P<0.05, ** P<0.01, *** P<0.001 vs. vehicle-treated Ctrl. LT4, 4-acetylantrocamol LT3; EMT, epithelial-mesenchymal transition; Ctrl, control.
Techniques Used: Migration, Colony Assay, Staining, Wound Healing Assay, Inhibition, Western Blot, Control
Figure Legend Snippet: Transcriptomic analysis of LT4-treated HCT116 cells reveals modulation of tumor-associated pathways. (A) Volcano plot illustrating DEGs in HCT116 cells treated with LT4 (10 μ M, 24 h) compared with the control. DEGs were defined using thresholds of |log 2 (fold change)|≥1 and adjusted P<0.05. Red dots indicate significantly upregulated genes; blue dots indicate significantly downregulated genes (adjusted P<0.05). (B) Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of DEGs. The x-axis represents the enrichment score, defined as the ratio of DEG counts to background counts for each pathway (log-transformed), with positive values indicating enrichment. Gene Ontology enrichment analysis of DEGs based on (C) Biological Process, (D) Molecular Function and (E) Cellular Component. Data are expressed as enrichment score or DEG counts. LT4, 4-acetylantrocamol LT3; DEGs, differentially expressed genes.
Techniques Used: Control, Transformation Assay
Figure Legend Snippet: PPI network and hub gene analysis of LT4-regulated DEGs in HCT116 cells. (A) PPI network of 63 DEGs (adjusted P<0.05) with non-zero node degree, constructed using the STRING database. Node-node interactions were filtered at a medium confidence level (interaction score ≥0.4). Known and predicted protein interactions are indicated by colored edges. (B) Network of key hub genes identified using CytoHubba topological analysis in Cytoscape. Node color intensity reflects centrality values (red=higher centrality). (C) MCODE analysis identified four gene clusters based on connectivity density. Each cluster is defined by its score (calculated as the product of subnetwork density and number of nodes), node count and edge count (number of interactions within the cluster). See for the full STRING node list and for detailed CytoHubba centrality rankings. PPI, protein-protein interaction; LT4, 4-acetylantrocamol LT3; DEGs, differentially expressed genes; MCODE, Molecular Complex Detection.
Techniques Used: Construct
Figure Legend Snippet: LT4 inhibits PI3K/AKT/mTOR signaling in HCT116 cells. (A) Western blot analysis of p-PI3K (p85, 85 kDa), total PI3K, p-AKT (Ser473, 60 kDa), total AKT, p-mTOR (289 kDa) and total mTOR in cells treated with LT4 (0.1, 1, 3 and 10 μ M) for 24 h. β-actin (45 kDa) served as the loading control. Semi-quantification of (B) p-mTOR/mTOR, (C) p-PI3K p85/PI3K p85 and (D) p-AKT (Ser473)/AKT. Data are presented as the mean ± SD from three independent experiments. Representative blots are shown; bar graphs represent densitometric quantification from three independent experiments (n=3), normalized to the indicated total protein, and expressed as fold change relative to the vehicle-treated Ctrl. * P<0.05, ** P<0.01, *** P<0.001 vs. vehicle-treated Ctrl. LT4, 4-acetylantrocamol LT3; p-, phosphorylated; Ctrl, control.
Techniques Used: Western Blot, Control
Figure Legend Snippet: LT4 modulates downstream PI3K/AKT signaling via FOXO3a, p27 kip1 , FOXO1 and GSK3β in HCT116 cells. HCT116 cells were treated with LT4 (0.1, 1, 3 and 10 μ M) for 24 h, followed by western blotting and densitometric analysis. (A) Representative western blots of FOXO3a (82-97 kDa) and p27 kip1 (27 kDa), with β-actin (45 kDa) as the loading control. (B) Densitometric quantification of FOXO3a/β-actin. (C) Densitometric quantification of p27 kip1 /β-actin. (D) Representative western blots of p-FOXO1 (Ser256), total FOXO1 (78-82 kDa), p-GSK3β (Ser9) and total GSK3β (46 kDa). β-actin (45 kDa) served as the loading control. (E) Densitometric quantification of p-FOXO1/FOXO1. (F) Densitometric quantification of p-GSK3β/GSK3β. Data are presented as the mean ± SD from three independent experiments. Bar graphs represent densitometric quantification from three independent experiments (n=3), normalized to the indicated total protein or β-actin, and expressed as fold change relative to the vehicle-treated Ctrl. * P<0.05, ** P<0.01 vs. vehicle-treated Ctrl. LT4, 4-acetylantrocamol LT3; p-, phosphorylated; Ctrl, control.
Techniques Used: Western Blot, Control
Figure Legend Snippet: LT4 modulates the MAPK signaling pathway and suppresses COX-2 protein expression in HCT116 cells. HCT116 cells were treated with LT4 (0.1, 1, 3 and 10 μ M) for 24 h. (A) Representative western blots of p-ERK1/2 (42/44 kDa), total ERK1/2 and p21 (21 kDa), with β-actin (45 kDa) as the loading control. (B) Densitometric quantification of p-ERK/ERK. (C) Densitometric quantification of p21/β-actin. (D) Representative western blots of p-p38 (43 kDa) and total p38 (40 kDa), with β-actin as the loading control, and corresponding densitometric quantification of p-p38/p38. (E) Representative western blot of COX-2 (74 kDa) with β-actin as the loading control. (F) Densitometric quantification of COX-2/β-actin. Data are presented as the mean ± SD from three independent experiments (n=3). Representative blots are shown; bar graphs represent densitometric quantification from three independent experiments (n=3), normalized to the indicated total protein or β-actin, and expressed as fold change relative to the vehicle-treated Ctrl. * P<0.05, ** P<0.01, *** P<0.001 vs. vehicle-treated Ctrl. LT4, 4-acetylantrocamol LT3; p-, phosphorylated; Ctrl, control; COX-2, cyclooxygenase-2.
Techniques Used: Expressing, Western Blot, Control
Figure Legend Snippet: LT4 induces a pro-apoptotic shift in Bcl-2 family protein levels and reduces the levels of the mitochondrial marker, COX IV, in HCT116 cells. HCT116 cells were treated with LT4 (0.1, 1, 3 and 10 μ M) for 24 h. (A) Representative immunoblots of Bcl-XL (30 kDa) and COX IV (17 kDa), with β-actin (45 kDa) serving as the loading control. (B) Densitometric quantification of Bcl-XL/β-actin. (C) Representative immunoblot and densitometric quantification of Bcl-2 (28 kDa)/β-actin. (D) Representative immunoblot and densitometric quantification of Bax (20 kDa)/β-actin. (E) Densitometric quantification of COX IV/β-actin. Data are presented as the mean ± SD from three independent experiments (n=3), normalized to β-actin and expressed as fold change relative to the vehicle-treated Ctrl. * P<0.05 vs. vehicle-treated Ctrl. LT4, 4-acetylantrocamol LT3; Ctrl, control; COX IV, cytochrome c oxidase subunit IV.
Techniques Used: Marker, Western Blot, Control
Figure Legend Snippet: Proposed schematic model of LT4-mediated anticancer signaling regulation in HCT116 colorectal cancer cells. This schematic summarizes the proposed major pathways and regulatory nodes modulated by LT4, based on transcriptomic, western blotting and molecular docking analyses. LT4 inhibits the PI3K/AKT/mTOR signaling cascade, as reflected by reduced phosphorylation signaling and the annotated functional outcomes (cell viability/cell proliferation and protein synthesis). In addition, LT4 shifts EMT marker expression toward an epithelial phenotype (increased E-cadherin and decreased N-cadherin). In parallel, LT4 modulates the GSK3β-FOXO1/FOXO3a node and differentially regulates MAPK signaling by suppressing ERK phosphorylation while enhancing p38 activation, accompanied by p21 upregulation, consistent with cell-cycle arrest and stress-response phenotypes. LT4 also modulates apoptosis by decreasing the levels of anti-apoptotic proteins (Bcl-2 and Bcl-XL) and increasing Bax expression, alongside mitochondrial destabilization (COX IV) and COX-2 suppression. Key hub genes identified through protein-protein interaction network analysis, SLC3A2, CCND1, PSAT1 and CHAC1, are highlighted as potential mediators linking transcriptomic regulation to these functional outcomes. Black arrows indicate canonical interactions supported by previous studies; red arrows indicate regulatory effects supported by the experimental data in the present study; dashed lines indicate docking-predicted interactions. Arrows indicate activation, whereas blunt-ended lines indicate inhibition. LT4, 4-acetylantrocamol LT3; PI3K, phosphoinositide 3-kinase; AKT, protein kinase B; mTOR, mechanistic target of rapamycin; MAPK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinase; GSK3β, glycogen synthase kinase 3 β; FOXO, forkhead box O; BAX, COX IV, cytochrome c oxidase subunit IV; COX-2, cyclooxygenase-2; N-cad, N-cadherin; E-cad, E-cadherin; EMT, epithelial-mesenchymal transition; P, phosphorylation; SLC3A2, solute carrier family 3 member 2; CCND1, cyclin D1; PSAT1, phosphoserine aminotransferase 1; CHAC1, ChaC glutathione-specific γ-glutamylcyclotransferase 1.
Techniques Used: Western Blot, Phospho-proteomics, Functional Assay, Marker, Expressing, Activation Assay, Inhibition
