Journal: International Journal of Molecular Sciences

Article Title: Epigenetic Silencing of miR-218-5p Modulates BIRC5 and DDX21 Expression to Promote Colorectal Cancer Progression

doi: 10.3390/ijms26094146

Figure Lengend Snippet: Validation of selected miR-218-5p Gene Targets. ( A ) Validation of BIRC5 and DDX21 as bona fide gene targets for miR-218-5p in CRC. Two-tailed t -test was used to compare different groups. ** p < 0.005, *** p < 0.0005, **** p < 0.00005. ( B ) Western blot showing DDX21 protein expression in miR-218-5p overexpressing compared to control HT-29 and HCT116 cells. Quantification of DDX21 protein expression normalized to ACTB is shown in the right panel. ( C ) Gene effect score based on CRISPR-Cas9 screen data in 40 CRC cell models from the DepMap database.

Article Snippet: A notable observation within SLIT2 , which encodes miR-218-1 within its intronic region, is the detection of higher levels of hypermethylation near the end of the promoter regions in the CRC cell lines, just upstream of the transcription start site, where the TATA box is typically located.

Techniques: Biomarker Discovery, Two Tailed Test, Western Blot, Expressing, Control, CRISPR

Journal: International Journal of Molecular Sciences

Article Title: Epigenetic Silencing of miR-218-5p Modulates BIRC5 and DDX21 Expression to Promote Colorectal Cancer Progression

doi: 10.3390/ijms26094146

Figure Lengend Snippet: Suppression of SLIT2 and SLIT3 miR-218 Host Genes in CRC. ( A ) Genomic location of miR-218-1 and miR-218-2 within the SLIT2 and SLIT3 genomic region on chromosome 4 and 5, respectively. ( B ) Correlation plot between miR-218-5p and SLIT2 ( left ) and SLIT3 ( right ) in a large cohort of COAD (n = 450) from the ENCORI project. ( C ) Downregulation of SLIT2 ( left ) and SLIT3 ( right ) in COAD (n = 275) compared to normal colon tissue (n = 349) from GEPIA2 database. T: tumor, N: normal. * p < 0.05. ( D ) Methylation analysis of SLIT2 and SLIT3 promoters using bisulfite conversion and NGS in a panel of CRC cell models (HCT116, HT-29, SW-480, LoVo, and DLD-1) compared to the MCF10A normal epithelial cells. ( E ) Schematic representation illustrating (🠯) downregulation of SLIT2 and SLIT3 in CRC to lead to miR-218-5p suppression (🠯), thus promoting tumorigenesis due to lifted suppression (🠭) of BIRC5, DDX21, and other gene targets identified in the current study.

Article Snippet: A notable observation within SLIT2 , which encodes miR-218-1 within its intronic region, is the detection of higher levels of hypermethylation near the end of the promoter regions in the CRC cell lines, just upstream of the transcription start site, where the TATA box is typically located.

Techniques: Methylation

Journal: Oncogenesis

Article Title: Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway

doi: 10.1038/oncsis.2017.84

Figure Lengend Snippet: Colorectal carcinoma CM enhanced the migration, invasion, tube formation and Dil-Ac-LDL uptake abilities of NECs. ( a ) NECs monolayer was wounded and induced by SW620, HT-29 or HCT116 CM. Photographs were taken after induction for 0, 24 and 48 h (scale bar 40 μm). ( b ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h. The number of invaded cells was counted in three random fields. Representative images of invaded cells were shown (scale bar 40 μm). ( c ) Formation tubes in each group were photographed. The number of tubes per field was counted in three random fields (scale bar 20 μm). ( d ) Representative images showed the Dil-Ac-LDL uptake ability of NECs and quantification of the relative Dil-Ac-LDL uptake (scale bar 40 μm). Data are presented as mean±s.d. from three independent experiments. *** P <0.001.

Article Snippet: The human colorectal cancer cell lines SW620, HT-29 and HCT116 were obtained from Nanjing Keygen Biotech Corp. (Nanjing, China), and cultured in RPMI-1640 (Biological Industries, Kibbutz Beit Haemek, Israel) medium with 10% fetal bovine serum.

Techniques: Migration

Journal: Oncogenesis

Article Title: Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway

doi: 10.1038/oncsis.2017.84

Figure Lengend Snippet: Colorectal carcinoma CM promoted the transition of NECs toward TECs. ( a ) Immunohistochemical staining for TECs markers (TEM1, TEM8 and VEGFR2) in colorectal carcinoma and peri-carcinoma tissue (scale bar 20 μm). ( b ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h. The relative mRNA levels of TECs markers were determined by qRT–PCR. ( c , d ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h, the protein levels of TECs markers were detected by western blot ( c ) and immunofluorescence ( d ). Data are presented as mean±s.d. from three independent experiments. ** P <0.01, *** P <0.001.

Article Snippet: The human colorectal cancer cell lines SW620, HT-29 and HCT116 were obtained from Nanjing Keygen Biotech Corp. (Nanjing, China), and cultured in RPMI-1640 (Biological Industries, Kibbutz Beit Haemek, Israel) medium with 10% fetal bovine serum.

Techniques: Immunohistochemical staining, Staining, Quantitative RT-PCR, Western Blot, Immunofluorescence

Journal: Oncogenesis

Article Title: Combination curcumin and (−)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway

doi: 10.1038/oncsis.2017.84

Figure Lengend Snippet: JAK/STAT3 signaling pathway was activated during the transition of NECs toward TECs induced by colorectal carcinoma CM. ( a ) NECs were induced by SW620, HT-29 or HCT116 CM for 48 h. The relative mRNA levels of JAK and STAT3 were measured by qRT–PCR. ( b , c ) The expression level of indicated protein was detected by western blot ( b ) and immunofluoresence (scale bar 50 μm) ( c ). Data are expressed as mean±s.d. from three independent experiments. * P <0.05, ** P <0.01, *** P <0.001.

Article Snippet: The human colorectal cancer cell lines SW620, HT-29 and HCT116 were obtained from Nanjing Keygen Biotech Corp. (Nanjing, China), and cultured in RPMI-1640 (Biological Industries, Kibbutz Beit Haemek, Israel) medium with 10% fetal bovine serum.

Techniques: Quantitative RT-PCR, Expressing, Western Blot

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Antitumor effect in LIM1215(A) xenografts by treatment received. (A and B) assessed by average tumor volume and (C) relative growth rate. Arrowheads indicate dosing. Arrows indicate sample harvesting. Data represent mean ± SE. ( n = 3–7. * P < .05). B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Outcome of immunohistochemistry for Ki-67 in LIM1215(B) xenograft sections. (A) Using vehicle control, (B) panitumumab-bevacizumab, (C) bevacizumab-panitumumab, and (D) bevacizumab-bevacizumab. (E) Proportion of Ki-67-positive cells in all treatment groups. Sections were IHC stained for Ki-67 (brown) and counterstained with hematoxylin (purple). Representative images of the sections are shown. Data in the graph represent the mean ± SE ( n = 6–8). ** P < .01. B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Immunohistochemistry, Control, Staining

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Levels of Phosphorylated Growth Factor Receptors in LIM1215(A) Xenografts Treated with PB, BP, and BB Relative to Vehicle Control

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Phospho-proteomics, Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Results of western blotting in LIM1215(B) xenografts. (A) EPHA2 and pEPHA2 with panitumumab-bevacizumab compared with bevacizumab-panitumumab. (B) EPHA2 and pEPHA2 with panitumumab-bevacizumab compared with bevacizumab-bevacizumab. (C) Phosphorylation of EPHA2 for panitumumab-bevacizumab compared with bevacizumab-panitumumab and (D) compared with bevacizumab-bevacizumab. (E) RSK and pRSK with panitumumab-bevacizumab compared with bevacizumab-panitumumab and (F) RSK and pRSK with panitumumab-bevacizumab compared with bevacizumab-bevacizumab. (G) Phosphorylation of RSK for panitumumab-bevacizumab compared with bevacizumab-panitumumab and (H) compared with bevacizumab-bevacizumab. Data represent mean ± SD ( n = 8). ** P < .01, *** P < .001. B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Western Blot, Phospho-proteomics, Control

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Enrichment Analysis of LIM1215(A) Xenografts Treated with Bevacizumab-Bevacizumab Compared with Vehicle Control (all Canonical Pathways, P < .001)

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Control, Activation Assay, Inhibition

Journal: Neoplasia (New York, N.Y.)

Article Title: Biologic Response of Colorectal Cancer Xenograft Tumors to Sequential Treatment with Panitumumab and Bevacizumab

doi: 10.1016/j.neo.2018.04.006

Figure Lengend Snippet: Relative expression of (A–H) lipogenic ( FASN, HMGCR, MVD, LSS ) and (I–L) hypoxia-related ( CA9, TGFBI ) genes in LIM1215(B) xenograft tumors. Expression relative to vehicle control with first-line treatment is shown in (A–D) and (I–J), and with sequential treatment in (E–H) and (K–L). Data represent mean ± SD ( n = 8). * P < .05, ** P < .01. B, bevacizumab; P, panitumumab; V, vehicle control.

Article Snippet: The human colon cancer cell line LIM1215 was obtained from the European Collection of Authenticated Cell Cultures (ECACC, Salisbury, UK).

Techniques: Expressing, Control

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Analysis of mutational burden in a panel of 64 CRC cell lines. Mutational characterization and comparison of SNVs and frameshifts among MSS (46 samples), MSI (12 samples), and POLE mutated (6 samples) of CRC models. a The distribution of SNVs per Mb of coding DNA at time 0 is shown for each cell line. b The number of frameshift mutations at time 0 is shown for each cell line. c The number of SNVs per each group is shown (“MSS” refers to MSS cells without POLE mutations; “MSI” includes MSI cells, as well as the SNU1040 cell line which is both MSI and POLE mutated; “POLE” includes only MSS cell lines carrying a POLE mutation). d The number of frameshifts per group is shown. The center line of each box plot indicates the median. p < 0.0001

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: Comparison, Mutagenesis

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: In vitro evolution of mutational landscape in 45 CRC cell lines. Mutational characterization of CRC cells after 90 days of culture (T90 ) in vitro. a Bar charts show the number of novel alterations (SNVs and frameshifts) acquired at T90 (not present at T0) for each cell line. b The number of predicted neoantigens (see the “ ” section) is shown. Each bar represents putative neoepitopes derived from SNVs and frameshifts

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: In Vitro, Immunopeptidomics, Derivative Assay

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Lost and gained mutations across evolving CRC cell lines. For each CRC model, the allelic frequency of SNVs at T0 and T90 are shown. Mutations were called against the reference genome (hg38) with allelic frequency > 1. The y -axis reports all the mutations found in each cell line, whereas the time points data are reported on x -axis

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques:

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Mutational signatures associated with alterations emerging during in vitro or in vivo CRC propagation. Analysis of 30 validated cancer-associated mutational signatures in hypermutated/rapidly evolving CRC cell lines. Signatures associated to MMR-deficient (6, 15, 20, 26), POLE -dependent (10), and MUTYH -associated polyposis (18) are highlighted. Analysis and clustering were performed as reported in the “Methods” section. a Heatmap of signature contributions during replication of CRC cells in vitro by analyzing alterations acquired at T90. b Heatmap of signature contributions during replication of the CRC cells in vivo by comparing xenograft tumors to the corresponding cells at T0 (see the “ ” section for detailed information)

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: In Vitro, In Vivo

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Analysis of cell ploidy in a panel of 64 CRC cell lines. Heatmap showing distribution of ploidy for every segmented region in each cell line. Samples are sorted from most to less mutated as reported in Fig. . The percentage (ploidy) is calculated as described in detail in the “Methods” section

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques:

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Transcriptional analysis of CRC cell lines. Differential expression analysis between hypermutated and non-hypermutated cells. a 183 unique genes differentially expressed between hypermutated (MSI/ POLE ) versus non-hypermutated CRC cells (MSS). Log2 expression values along with the mean change in expression are shown. b Pathway analysis of genes differentially expressed between hypermutated versus non-hypermutated CRC cells using g:Profiler application (see the “ ” section)

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: Quantitative Proteomics, Expressing

Journal: Genome Medicine

Article Title: Evolving neoantigen profiles in colorectal cancers with DNA repair defects

doi: 10.1186/s13073-019-0654-6

Figure Lengend Snippet: Beta2 microglobulin (B2M) expression is downregulated in EVOLVING-CRC. Transcriptional and protein levels of the B2M gene. a Genes differentially expressed in EVOLVING-CRC relative to STABLE-CRC with a significant p value ( p < 0.05). b Waterfall chart showing B2M expression at RNA level across a panel of 45 CRC cell lines. c Western blot analysis of B2M expression. In gray are highlighted samples for which T90 sequencing were not available. Blots were reprobed with anti-HSP90 antibody to confirm equal loading. d B2M gene alterations on 64 CRC cell lines at T0 (upper panel) and codon affected (lower panel)

Article Snippet: Each CRC cell line (5 × 10 6 cells) was injected subcutaneously into both flanks of two 6-week-old female NOD (nonobese diabetic)/SCID (severe combined immunodeficient) mice (Charles River Laboratory).

Techniques: Expressing, Western Blot, Sequencing

Journal: Oncology Reports

Article Title: Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1

doi: 10.3892/or.2024.8741

Figure Lengend Snippet: Clinical significance of ZNF169 in patients with CRC. (A) The transcript abundance of ZNF169 was analyzed in CRC tissues (n=286) and adjacent normal tissues (n=41) based on TCGA database. P<0.05. (B) Immunohistochemical staining of ZNF169 in a tissue microarray containing CRC and adjacent normal tissues. (C) Overall survival of CRC patients who were divided into the ZNF169 high (n=161) and low (n=161) expression groups. P=0.034. (D) The protein expression of ZNF169 was examined using western blot analysis in the normal colon cell line NCM460, and in the CRC cells, RKO, HCT-116, SW620, HT-29 and HCT-8. During the western blot analysis experiments, the blots were cut prior to incubation with the antibodies. ZNF169, zinc finger protein 169; CRC, colorectal cancer; TCGA, The Cancer Genome Atlas.

Article Snippet: The CRC cell lines, RKO (cat no. CL-0196), HCT-116 (cat no. CL-0096), HT-29 (cat no. CL-0118), SW620 (cat no. CL-0225) and HCT-8 (cat no. CL-0098), were purchased from Procell Life Science & Technology Co. Ltd. STR profiling was used to confirm the authentication of the HT-29 cell line.

Techniques: Immunohistochemical staining, Staining, Microarray, Expressing, Western Blot, Incubation

Journal: Oncology Reports

Article Title: Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1

doi: 10.3892/or.2024.8741

Figure Lengend Snippet: ZNF169 promotes the proliferation of colorectal cancer cells. (A) Western blot analysis of ZNF169 in siCtrl- and siZNF169-transfected HCT-116 and RKO cells. (B) CCK-8 assay was applied to detect the viability of the siCtrl- and siZNF169-transfected HCT-116 and RKO cells. *P<0.05 and **P<0.01, vs. the control. (C) Colony formation assay was performed in the siCtrl- and siZNF169-transfected HCT-116 and RKO cells. *P<0.05 and **P<0.01, vs. the control. (D) Western blot analysis of ZNF169 expression in HT-29 cells transfected with Ctrl and ZNF169-overexpressing lentivirus. (E) CCK-8 assay was applied to detect the viability of the Ctrl and ZNF169-overexpressing HT-29 cells. *P<0.05 and **P<0.01, vs. the control. (F) Colony formation assay was performed in the Ctrl and ZNF169-overexpressing HT-29 cells. **P<0.01, vs. the control. During the western blot analysis experiments, the blots were cut prior to incubation with the antibodies. The results are presented as the mean ± standard error of the mean. ZNF169, zinc finger protein 169.

Article Snippet: The CRC cell lines, RKO (cat no. CL-0196), HCT-116 (cat no. CL-0096), HT-29 (cat no. CL-0118), SW620 (cat no. CL-0225) and HCT-8 (cat no. CL-0098), were purchased from Procell Life Science & Technology Co. Ltd. STR profiling was used to confirm the authentication of the HT-29 cell line.

Techniques: Western Blot, Transfection, CCK-8 Assay, Control, Colony Assay, Expressing, Incubation

Journal: Oncology Reports

Article Title: Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1

doi: 10.3892/or.2024.8741

Figure Lengend Snippet: ZNF169 affects EdU staining and caspase-3/7 activity in colorectal cancer cells. (A and B) EdU staining was performed in siCtrl and siZNF169-transfected HCT-116 and RKO cells, and in Ctrl and ZNF169-overexpressing HT-29 cells. *P<0.05, vs. the control. (C) Caspase-3/7 activity was analyzed in the siCtrl and siZNF169-transfected HCT-116 and RKO cells, and in Ctrl and ZNF169-overexpressing HT-29 cells. *P<0.05, vs. the control. The results are presented as the mean ± standard error of the mean. ZNF169, zinc finger protein 169.

Article Snippet: The CRC cell lines, RKO (cat no. CL-0196), HCT-116 (cat no. CL-0096), HT-29 (cat no. CL-0118), SW620 (cat no. CL-0225) and HCT-8 (cat no. CL-0098), were purchased from Procell Life Science & Technology Co. Ltd. STR profiling was used to confirm the authentication of the HT-29 cell line.

Techniques: Staining, Activity Assay, Transfection, Control

Journal: Oncology Reports

Article Title: Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1

doi: 10.3892/or.2024.8741

Figure Lengend Snippet: ZNF169 potentiates the transcriptional activity of the ANKZF1 gene in CRC cells. (A) The positively correlated genes of ZNF169 were analyzed in patients with CRC based on The Cancer Genome Atlas database. (B) Reverse transcription-quantitative PCR assay was used to detect the mRNA expression levels of ANKZF1 in siCtrl and siZNF169-transfected HCT-116 cells and RKO cells, and in Ctrl and ZNF169-overexpressing HT-29 cells. *P<0.05, vs. the control. (C) Western blot analysis was used to detect the protein expression levels of ANKZF1 in siCtrl and siZNF169-transfected HCT-116 cells, and in Ctrl and ZNF169-overexpressing HT-29 cells. (D) Dual luciferase activity was detected in siCtrl and siZNF169-transfected HCT-116 cells, and in Ctrl and ZNF169-overexpressing HT-29 cells. *P<0.05, vs. the control. (E) Chromatin immunoprecipitation-quantitative PCR was performed to analyze the interaction between ZNF169 and the promoter sequence of ANKZF1 in CRC cells. **P<0.01, vs. the control. During the western blot analysis experiments, the blots were cut prior to incubation with the antibodies. The results are presented as the mean ± standard error of the mean. ZNF169, zinc finger protein 169; CRC, colorectal cancer; ANKZF1, ankyrin repeat and zinc-finger domain-containing 1.

Article Snippet: The CRC cell lines, RKO (cat no. CL-0196), HCT-116 (cat no. CL-0096), HT-29 (cat no. CL-0118), SW620 (cat no. CL-0225) and HCT-8 (cat no. CL-0098), were purchased from Procell Life Science & Technology Co. Ltd. STR profiling was used to confirm the authentication of the HT-29 cell line.

Techniques: Activity Assay, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Transfection, Control, Western Blot, Luciferase, Chromatin Immunoprecipitation, Sequencing, Incubation