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ATCC human nb cell lines be 2 c

(A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified <t>(BE(2)-C,</t> LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).

Human Nb Cell Lines Be 2 C, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 441 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma"

Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

Journal: Cancer letters

doi: 10.1016/j.canlet.2026.218383

Figure Legend Snippet: (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).

Techniques Used: Gene Expression, Quantitative Proteomics, Biomarker Discovery, Expressing, Western Blot, Amplification

(A, B) BE(2)-C and SK-N-DZ cells were treated with doxorubicin (A) or etoposide (B), either individually or in combination with peposertib. Clonogenic assay was performed to evaluate long-term cell viability of NB cells. BE(2)-C and SK-N-DZ cells were treated with peposertib (1000 nM), and doxorubicin (BE(2)-C, 75 nM; SK-N-DZ, 10 nM) and etoposide (BE(2)-C, 500 nM; SK-N-DZ, 100 nM). Drugs were removed and replaced with fresh media 48 h later, and colonies were allowed to grow for 14 days. (C, D) DNA damage following doxorubicin (C) or etoposide (D) therapy in combination with peposertib was evaluated in BE(2)C and SK-N-DZ using immunofluorescence staining of γ-H2AX (Ser139) (Red: γ-H2AX; Blue: DAPI; Green: Phalloidin). (E) Clonogenic assay was performed to evaluate long-term viability of NB cells. BE(2)-C NTC and PRKDC knockdown cells were treated with etoposide (500 nM) and doxorubicin (75 nM). Drugs were removed and replaced with fresh media 48 h later, and colonies were allowed to grow for 14 days; *p<0.05, ***p<0.001, ****p<0.0001.

Figure Legend Snippet: (A, B) BE(2)-C and SK-N-DZ cells were treated with doxorubicin (A) or etoposide (B), either individually or in combination with peposertib. Clonogenic assay was performed to evaluate long-term cell viability of NB cells. BE(2)-C and SK-N-DZ cells were treated with peposertib (1000 nM), and doxorubicin (BE(2)-C, 75 nM; SK-N-DZ, 10 nM) and etoposide (BE(2)-C, 500 nM; SK-N-DZ, 100 nM). Drugs were removed and replaced with fresh media 48 h later, and colonies were allowed to grow for 14 days. (C, D) DNA damage following doxorubicin (C) or etoposide (D) therapy in combination with peposertib was evaluated in BE(2)C and SK-N-DZ using immunofluorescence staining of γ-H2AX (Ser139) (Red: γ-H2AX; Blue: DAPI; Green: Phalloidin). (E) Clonogenic assay was performed to evaluate long-term viability of NB cells. BE(2)-C NTC and PRKDC knockdown cells were treated with etoposide (500 nM) and doxorubicin (75 nM). Drugs were removed and replaced with fresh media 48 h later, and colonies were allowed to grow for 14 days; *p<0.05, ***p<0.001, ****p<0.0001.

Techniques Used: Clonogenic Assay, Immunofluorescence, Staining, Knockdown

(A) BE(2)-C GFP-Luc cells were intravenously injected into NOD rag gamma mice. Chemotherapy commenced 6 days post-injection, with q.o.d doxorubicin (2.5 mg/kg, iv) and peposertib (100 mg/kg, gavage) as combination therapy, followed by a single dose of peposertib alone (100 mg/kg) the next day. Bioluminescent imaging (top) and GFP imaging (bottom) to demonstrate therapy outcomes on liver metastasis burden. (B) Bioluminescent signal quantification was used to measure liver metastasis burden at the end of the study (*p<0.05). (C) Gross photograph of GI track in doxorubicin and peposertib combination. (D) Mouse weight.

Figure Legend Snippet: (A) BE(2)-C GFP-Luc cells were intravenously injected into NOD rag gamma mice. Chemotherapy commenced 6 days post-injection, with q.o.d doxorubicin (2.5 mg/kg, iv) and peposertib (100 mg/kg, gavage) as combination therapy, followed by a single dose of peposertib alone (100 mg/kg) the next day. Bioluminescent imaging (top) and GFP imaging (bottom) to demonstrate therapy outcomes on liver metastasis burden. (B) Bioluminescent signal quantification was used to measure liver metastasis burden at the end of the study (*p<0.05). (C) Gross photograph of GI track in doxorubicin and peposertib combination. (D) Mouse weight.

Techniques Used: Injection, Imaging

(A) BE(2)-C cells were pre-treated with peposertib for 30 min before IR, then cells were irradiated at 1 Gy and peposertib was removed at different time points (top panel). BE(2)-C cells were irradiated at 1 Gy and peposertib was added at different time points post-IR (bottom panel). (B) Colony viability was measured by colony formation assay. (C) BE2C cells were cultured for 7 days to form colonies before initiating doxorubicin (75 and 150 nM) or IR (1 Gy and 4 Gy) therapy alone or in combination with peposertib. Following treatment, the media was refreshed 48 h later, and the colonies were permitted to grow for an additional 7 days. (D) Colony viability was measured by colony formation assay. (E) Similarly, SK-N-DZ cells were allowed to form colonies for 7 days prior to treatment with doxorubicin (10 or 20 nM) or ionizing radiation (0.5 Gy or 2 Gy), alone or in combination with peposertib. The culture medium was refreshed 48 h post-treatment, and colonies were incubated for an additional 7 days. (F) Represents the Colony viability measurement.; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Figure Legend Snippet: (A) BE(2)-C cells were pre-treated with peposertib for 30 min before IR, then cells were irradiated at 1 Gy and peposertib was removed at different time points (top panel). BE(2)-C cells were irradiated at 1 Gy and peposertib was added at different time points post-IR (bottom panel). (B) Colony viability was measured by colony formation assay. (C) BE2C cells were cultured for 7 days to form colonies before initiating doxorubicin (75 and 150 nM) or IR (1 Gy and 4 Gy) therapy alone or in combination with peposertib. Following treatment, the media was refreshed 48 h later, and the colonies were permitted to grow for an additional 7 days. (D) Colony viability was measured by colony formation assay. (E) Similarly, SK-N-DZ cells were allowed to form colonies for 7 days prior to treatment with doxorubicin (10 or 20 nM) or ionizing radiation (0.5 Gy or 2 Gy), alone or in combination with peposertib. The culture medium was refreshed 48 h post-treatment, and colonies were incubated for an additional 7 days. (F) Represents the Colony viability measurement.; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Techniques Used: Irradiation, Colony Assay, Cell Culture, Incubation

(A) Area of irradiation outlined by a light window. (B) BE(2)-C GFP-Luc cells were injected iv into NOD rag gamma mice. Radiation therapy started 6 days after cancer cell injection with daily 2 Gy irradiation alone or in combination with peposertib (gavage; 100 mg/kg) for 4 days. (C) Bioluminescent imaging and (D) GFP imaging demonstrate therapy outcomes on liver metastasis burden. (E) Bioluminescent signal quantification to measure liver metastasis burden at the end of the study (*p < 0.05). (F) Mouse weight. (G) Gross photograph of liver metastasis. (H) H&E imaging of liver metastasis and normal liver adjacent to metastatic tumors. (I ) DNA-PKcs expression in surviving colonies after acute (5 Gy) and chronic (1 Gy × 5 times) IR exposure. (J ) BE(2)-C cells subjected to repeated low-dose irradiation (1 Gy × 5) exhibited increased resistance to acute high-dose radiotherapy (5 Gy) relative to the parental cell line. (K ) PRKDC gene expression in NB tumors with recurrence or progression (Versteeg study, n = 87) revealed a significant upregulation of PRKDC in tumors at relapse. (L) Side-by-side UMAP visualization of NB tumor cell subclusters in post-treatment neuroblastoma at primary (n = 21,248 cells) and metastatic (n = 24,526 cells) sites after re-clustering. Colors represent assigned cell types within NB tumors. The dot plot shows PRKDC gene expression in tumor subpopulations in NB at primary and metastatic locations post-induction treatment. The color scale represents scaled average expression of PRKDC in each tumor type, and the size of the circle indicates the proportion of cells expressing PRKDC . (M) DNA-PKcs inhibition in combination with radiotherapy disrupts self-renewal capacity of BE(2)-C cells. BE(2)-C cells were treated with 5 cycles of doxorubicin (50 nM) therapy or irradiation (1 Gy) alone or in combination with peposertib. (N) Elevated DNA-PKcs expression in metastatic NB cells confers a survival advantage under chemotherapeutic and radiotherapeutic stress. DNA-PKcs inhibition combined with repeated low-dose ionizing radiation impairs cancer cell self-renewal capacity and suppresses tumor relapse.

Figure Legend Snippet: (A) Area of irradiation outlined by a light window. (B) BE(2)-C GFP-Luc cells were injected iv into NOD rag gamma mice. Radiation therapy started 6 days after cancer cell injection with daily 2 Gy irradiation alone or in combination with peposertib (gavage; 100 mg/kg) for 4 days. (C) Bioluminescent imaging and (D) GFP imaging demonstrate therapy outcomes on liver metastasis burden. (E) Bioluminescent signal quantification to measure liver metastasis burden at the end of the study (*p < 0.05). (F) Mouse weight. (G) Gross photograph of liver metastasis. (H) H&E imaging of liver metastasis and normal liver adjacent to metastatic tumors. (I ) DNA-PKcs expression in surviving colonies after acute (5 Gy) and chronic (1 Gy × 5 times) IR exposure. (J ) BE(2)-C cells subjected to repeated low-dose irradiation (1 Gy × 5) exhibited increased resistance to acute high-dose radiotherapy (5 Gy) relative to the parental cell line. (K ) PRKDC gene expression in NB tumors with recurrence or progression (Versteeg study, n = 87) revealed a significant upregulation of PRKDC in tumors at relapse. (L) Side-by-side UMAP visualization of NB tumor cell subclusters in post-treatment neuroblastoma at primary (n = 21,248 cells) and metastatic (n = 24,526 cells) sites after re-clustering. Colors represent assigned cell types within NB tumors. The dot plot shows PRKDC gene expression in tumor subpopulations in NB at primary and metastatic locations post-induction treatment. The color scale represents scaled average expression of PRKDC in each tumor type, and the size of the circle indicates the proportion of cells expressing PRKDC . (M) DNA-PKcs inhibition in combination with radiotherapy disrupts self-renewal capacity of BE(2)-C cells. BE(2)-C cells were treated with 5 cycles of doxorubicin (50 nM) therapy or irradiation (1 Gy) alone or in combination with peposertib. (N) Elevated DNA-PKcs expression in metastatic NB cells confers a survival advantage under chemotherapeutic and radiotherapeutic stress. DNA-PKcs inhibition combined with repeated low-dose ionizing radiation impairs cancer cell self-renewal capacity and suppresses tumor relapse.

Techniques Used: Irradiation, Injection, Imaging, Expressing, Gene Expression, Inhibition

Image Search Results

Journal: Cancer letters

Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

doi: 10.1016/j.canlet.2026.218383

Figure Lengend Snippet: (A, B) Correlation between PRKDC gene expression levels and NB tumor progression to stage 4. (C) Heatmap of differential expression of DNA replication and repair pathway (KEGG) genes in PTCs (green) at diagnosis and DTCs (red) at relapse. Color intensity represents expression level. Heatmap of KEGG pathways involved in DNA replication and repair in primary tumor cells (PTCs) at diagnosis (green) and in disseminated tumors cells (DTCs) at relapse (red). (D) PRKDC gene expression in PTCs at diagnosis, DTCs at diagnosis and in DTCs at relapse (Ambros study, n=86) revealed a significant upregulation of PRKDC in DTCs at relapse. (E) Western blot analysis in MYCN-amplified (BE(2)-C, LAN-1, IMR-32 and SK-N-DZ) and MYCN-non-amplified (SK-N-AS, SK-N-SH) NB cell lines (*p<0.05, ***p<0.001, ****p<0.0001).

Article Snippet: MYCN -amplified human NB cell lines (BE(2)-C (CVCL_V006), IMR-32 (CVCL_0346), LAN-1 (CVCL_1827) and SK-N-DZ (CVCL_1701)) and MYCN -non-amplified cells (SK-N-AS (CVCL_1700), and SK-N-SH (CVCL_0531)) were purchased from ATCC.

Techniques: Gene Expression, Quantitative Proteomics, Biomarker Discovery, Expressing, Western Blot, Amplification

Journal: Cancer letters

Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

doi: 10.1016/j.canlet.2026.218383

Figure Lengend Snippet: (A, B) BE(2)-C and SK-N-DZ cells were treated with doxorubicin (A) or etoposide (B), either individually or in combination with peposertib. Clonogenic assay was performed to evaluate long-term cell viability of NB cells. BE(2)-C and SK-N-DZ cells were treated with peposertib (1000 nM), and doxorubicin (BE(2)-C, 75 nM; SK-N-DZ, 10 nM) and etoposide (BE(2)-C, 500 nM; SK-N-DZ, 100 nM). Drugs were removed and replaced with fresh media 48 h later, and colonies were allowed to grow for 14 days. (C, D) DNA damage following doxorubicin (C) or etoposide (D) therapy in combination with peposertib was evaluated in BE(2)C and SK-N-DZ using immunofluorescence staining of γ-H2AX (Ser139) (Red: γ-H2AX; Blue: DAPI; Green: Phalloidin). (E) Clonogenic assay was performed to evaluate long-term viability of NB cells. BE(2)-C NTC and PRKDC knockdown cells were treated with etoposide (500 nM) and doxorubicin (75 nM). Drugs were removed and replaced with fresh media 48 h later, and colonies were allowed to grow for 14 days; *p<0.05, ***p<0.001, ****p<0.0001.

Techniques: Clonogenic Assay, Immunofluorescence, Staining, Knockdown

Journal: Cancer letters

Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

doi: 10.1016/j.canlet.2026.218383

Figure Lengend Snippet: (A) BE(2)-C GFP-Luc cells were intravenously injected into NOD rag gamma mice. Chemotherapy commenced 6 days post-injection, with q.o.d doxorubicin (2.5 mg/kg, iv) and peposertib (100 mg/kg, gavage) as combination therapy, followed by a single dose of peposertib alone (100 mg/kg) the next day. Bioluminescent imaging (top) and GFP imaging (bottom) to demonstrate therapy outcomes on liver metastasis burden. (B) Bioluminescent signal quantification was used to measure liver metastasis burden at the end of the study (*p<0.05). (C) Gross photograph of GI track in doxorubicin and peposertib combination. (D) Mouse weight.

Techniques: Injection, Imaging

Journal: Cancer letters

Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

doi: 10.1016/j.canlet.2026.218383

Figure Lengend Snippet: (A) BE(2)-C cells were pre-treated with peposertib for 30 min before IR, then cells were irradiated at 1 Gy and peposertib was removed at different time points (top panel). BE(2)-C cells were irradiated at 1 Gy and peposertib was added at different time points post-IR (bottom panel). (B) Colony viability was measured by colony formation assay. (C) BE2C cells were cultured for 7 days to form colonies before initiating doxorubicin (75 and 150 nM) or IR (1 Gy and 4 Gy) therapy alone or in combination with peposertib. Following treatment, the media was refreshed 48 h later, and the colonies were permitted to grow for an additional 7 days. (D) Colony viability was measured by colony formation assay. (E) Similarly, SK-N-DZ cells were allowed to form colonies for 7 days prior to treatment with doxorubicin (10 or 20 nM) or ionizing radiation (0.5 Gy or 2 Gy), alone or in combination with peposertib. The culture medium was refreshed 48 h post-treatment, and colonies were incubated for an additional 7 days. (F) Represents the Colony viability measurement.; *p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Techniques: Irradiation, Colony Assay, Cell Culture, Incubation

Journal: Cancer letters

Article Title: DNA-PKcs promotes therapy resistance and metastatic recurrence in neuroblastoma

doi: 10.1016/j.canlet.2026.218383

Figure Lengend Snippet: (A) Area of irradiation outlined by a light window. (B) BE(2)-C GFP-Luc cells were injected iv into NOD rag gamma mice. Radiation therapy started 6 days after cancer cell injection with daily 2 Gy irradiation alone or in combination with peposertib (gavage; 100 mg/kg) for 4 days. (C) Bioluminescent imaging and (D) GFP imaging demonstrate therapy outcomes on liver metastasis burden. (E) Bioluminescent signal quantification to measure liver metastasis burden at the end of the study (*p < 0.05). (F) Mouse weight. (G) Gross photograph of liver metastasis. (H) H&E imaging of liver metastasis and normal liver adjacent to metastatic tumors. (I ) DNA-PKcs expression in surviving colonies after acute (5 Gy) and chronic (1 Gy × 5 times) IR exposure. (J ) BE(2)-C cells subjected to repeated low-dose irradiation (1 Gy × 5) exhibited increased resistance to acute high-dose radiotherapy (5 Gy) relative to the parental cell line. (K ) PRKDC gene expression in NB tumors with recurrence or progression (Versteeg study, n = 87) revealed a significant upregulation of PRKDC in tumors at relapse. (L) Side-by-side UMAP visualization of NB tumor cell subclusters in post-treatment neuroblastoma at primary (n = 21,248 cells) and metastatic (n = 24,526 cells) sites after re-clustering. Colors represent assigned cell types within NB tumors. The dot plot shows PRKDC gene expression in tumor subpopulations in NB at primary and metastatic locations post-induction treatment. The color scale represents scaled average expression of PRKDC in each tumor type, and the size of the circle indicates the proportion of cells expressing PRKDC . (M) DNA-PKcs inhibition in combination with radiotherapy disrupts self-renewal capacity of BE(2)-C cells. BE(2)-C cells were treated with 5 cycles of doxorubicin (50 nM) therapy or irradiation (1 Gy) alone or in combination with peposertib. (N) Elevated DNA-PKcs expression in metastatic NB cells confers a survival advantage under chemotherapeutic and radiotherapeutic stress. DNA-PKcs inhibition combined with repeated low-dose ionizing radiation impairs cancer cell self-renewal capacity and suppresses tumor relapse.

Techniques: Irradiation, Injection, Imaging, Expressing, Gene Expression, Inhibition

$(A) General Synthesis of QW-5–70. i). 60% NaH, SEMCl, THF, 0–25 °C; ii). n-BuLi, 3,4,5-trimethoxybenzaldehyde, THF, −78 °C; iii). Dess-Martin, CH 2 Cl 2 , r.t.; iv)1-(phenylsulfonyl)-4-(4,4,5,5-tetramethyl-1,3,2-dioxaborolan-2-yl)-1H-indazole, Pd(PPh 3 ) 4 , Na 2 CO 3 , 1,4-dioxane/H 2 O (v/v = 2/1), reflux; v). Pd(OAC) 2 , PPh 3 , K 2 CO 3 , n-butanol, reflux; vi). 37% HCl, MeOH, reflux. (B) QW-5–70 induced tubulin depolymerization. Colchicine and paclitaxel were included as reference compounds. (C) SPR sensorgrams of QW-5–70 and colchicine binding to tubulin. (mean ± SEM, n = 3) (D) EBI competition assays. The upper β-tubulin band represents native β-tubulin, while the lower band corresponds to the EBI–β-tubulin adduct. GAPDH served as a loading control. (E) Immunoblot analysis of soluble and polymerized β-tubulin in PC-3 cells following treatment with QW-5–70, colchicine, or paclitaxel (20 nM). Cells were fractionated into soluble and polymerized tubulin pools, which were analyzed by immunoblotting. Ponceau S staining and GAPDH were used as loading controls for polymerized and soluble fractions, respectively. Quantification of polymerized β-tubulin expressed as a percentage of total β-tubulin (soluble + polymerized). (mean ± SEM, n=3). (F) Representative immunofluorescence images of interphase and mitotic SK-N-BE(2)-C, NB-1691, and PC-3 cells treated with QW-5–70 (2 nM and 5 nM) for 24 h. Microtubules were stained with anti-α-tubulin antibodies (red), and nuclei were counterstained with DAPI (blue). Scale bar = 50 μm (n=3). (G) High-resolution X-ray crystal structure of the sT2R complex with QW-5–70. Left panel: detailed interactions of QW-5–70 (green sticks) within the colchicine-binding site are shown. Bound water molecules are represented as red spheres, and hydrogen bonds are indicated by dashed magenta lines. The electron density for QW-5–70 is shown as a blue mesh; the final 2Fo-Fc map is contoured at 1.0 σ. Middle panel: detailed interactions of colchicine (light-brown sticks) binding to sT2R (PDB 6XER) for comparison. Right panel: superposition of sT2R complexes with QW-5–70 and colchicine sT2R (colored grey) complexes, highlighting the relative inhibitor binding positions and differing conformations of the α-T5 and β-T7 loops.$

Journal: Molecular cancer therapeutics

Article Title: QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp–overexpressing cancer models

doi: 10.1158/1535-7163.MCT-25-1013

Figure Lengend Snippet: (A) General Synthesis of QW-5–70. i). 60% NaH, SEMCl, THF, 0–25 °C; ii). n-BuLi, 3,4,5-trimethoxybenzaldehyde, THF, −78 °C; iii). Dess-Martin, CH 2 Cl 2 , r.t.; iv)1-(phenylsulfonyl)-4-(4,4,5,5-tetramethyl-1,3,2-dioxaborolan-2-yl)-1H-indazole, Pd(PPh 3 ) 4 , Na 2 CO 3 , 1,4-dioxane/H 2 O (v/v = 2/1), reflux; v). Pd(OAC) 2 , PPh 3 , K 2 CO 3 , n-butanol, reflux; vi). 37% HCl, MeOH, reflux. (B) QW-5–70 induced tubulin depolymerization. Colchicine and paclitaxel were included as reference compounds. (C) SPR sensorgrams of QW-5–70 and colchicine binding to tubulin. (mean ± SEM, n = 3) (D) EBI competition assays. The upper β-tubulin band represents native β-tubulin, while the lower band corresponds to the EBI–β-tubulin adduct. GAPDH served as a loading control. (E) Immunoblot analysis of soluble and polymerized β-tubulin in PC-3 cells following treatment with QW-5–70, colchicine, or paclitaxel (20 nM). Cells were fractionated into soluble and polymerized tubulin pools, which were analyzed by immunoblotting. Ponceau S staining and GAPDH were used as loading controls for polymerized and soluble fractions, respectively. Quantification of polymerized β-tubulin expressed as a percentage of total β-tubulin (soluble + polymerized). (mean ± SEM, n=3). (F) Representative immunofluorescence images of interphase and mitotic SK-N-BE(2)-C, NB-1691, and PC-3 cells treated with QW-5–70 (2 nM and 5 nM) for 24 h. Microtubules were stained with anti-α-tubulin antibodies (red), and nuclei were counterstained with DAPI (blue). Scale bar = 50 μm (n=3). (G) High-resolution X-ray crystal structure of the sT2R complex with QW-5–70. Left panel: detailed interactions of QW-5–70 (green sticks) within the colchicine-binding site are shown. Bound water molecules are represented as red spheres, and hydrogen bonds are indicated by dashed magenta lines. The electron density for QW-5–70 is shown as a blue mesh; the final 2Fo-Fc map is contoured at 1.0 σ. Middle panel: detailed interactions of colchicine (light-brown sticks) binding to sT2R (PDB 6XER) for comparison. Right panel: superposition of sT2R complexes with QW-5–70 and colchicine sT2R (colored grey) complexes, highlighting the relative inhibitor binding positions and differing conformations of the α-T5 and β-T7 loops.

Article Snippet: Human neuroblastoma (NB) cell lines (SK-N-BE(2)-C, RRID: CVCL_0529; NB-1691, RRID: CVCL_5628; SK-N-BE(2), RRID: CVCL_0528; SiMa, RRID: CVCL_1695; IMR-32, RRID: CVCL_0346) and prostate cancer cell lines (PC-3, RRID: CVCL_0035; 22Rv1, RRID: CVCL_1045) were originally obtained from ATCC in 2019.

Techniques: Binding Assay, Reflux, Control, Western Blot, Staining, Immunofluorescence, Comparison

(A) Representative images and quantification of colony formation in BE2C/VCR cells treated with QW-5–70, vincristine, or colchicine (1–5 nM). (B) Colony formation assays in PC-3/TxR cells treated with QW-5–70, paclitaxel, or colchicine (1–5 nM). Colony area is expressed as mean ± SEM relative to vehicle control (n = 5). (C) Transwell migration of BE2C/VCR (left) and PC-3/TxR (right) cells after 24 h treatment with vincristine or paclitaxel (5 nM) or QW-5–70 (2 or 5 nM). (D) Transwell migration of BE2C/VCR (left) and PC-3/TxR (right) cells treated with QW-5–70 (0.5–5 nM) for 24 h. Migration area is expressed as mean ± SEM relative to control (n = 5). Scale bar = 100 μm. (E) Immunoblot analysis of P-gp expression in SK-N-BE(2)-C and BE2C/VCR cells. (F) Viability of BE2C/VCR cells treated with QW-5–70 or vincristine (0.1 nM–3 μM) in the absence or presence of verapamil (10 μM) for 72 h (MTS assay; n = 4). (G) Intracellular concentrations of QW-5–70 and vincristine in parental SK-N-BE(2)-C and BE2C/VCR cells following 50 nM, 2 h treatment, with or without tariquidar (1 μM), quantified by LC–MS/MS (n = 3). (H) Immunoblot analysis of P-gp expression in PC-3 and PC-3/TxR cells. (I) Cell viability of PC-3/TxR cells treated with QW-5–70 or paclitaxel (0.1 nM–3 μM) in the absence or presence of verapamil (10 μM) for 72 h (MTS assay; n = 4). (J) Intracellular concentrations of QW-5–70 and paclitaxel in PC-3 and PC-3/TxR cells under the same conditions as panel G, quantified by LC–MS/MS (n = 3). (K) Immunoblot analysis of P-gp expression in PC-3/TxR cells following transfection with scrambled control or si-P-gp. GAPDH served as a loading control. (L) Viability of QW-5–70 and paclitaxel in PC-3/TxR, PC-3/TxR-scramble, and PC-3/TxR-si-P-gp cells (MTS assay; n=4).

Journal: Molecular cancer therapeutics

Article Title: QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp–overexpressing cancer models

doi: 10.1158/1535-7163.MCT-25-1013

Figure Lengend Snippet: (A) Representative images and quantification of colony formation in BE2C/VCR cells treated with QW-5–70, vincristine, or colchicine (1–5 nM). (B) Colony formation assays in PC-3/TxR cells treated with QW-5–70, paclitaxel, or colchicine (1–5 nM). Colony area is expressed as mean ± SEM relative to vehicle control (n = 5). (C) Transwell migration of BE2C/VCR (left) and PC-3/TxR (right) cells after 24 h treatment with vincristine or paclitaxel (5 nM) or QW-5–70 (2 or 5 nM). (D) Transwell migration of BE2C/VCR (left) and PC-3/TxR (right) cells treated with QW-5–70 (0.5–5 nM) for 24 h. Migration area is expressed as mean ± SEM relative to control (n = 5). Scale bar = 100 μm. (E) Immunoblot analysis of P-gp expression in SK-N-BE(2)-C and BE2C/VCR cells. (F) Viability of BE2C/VCR cells treated with QW-5–70 or vincristine (0.1 nM–3 μM) in the absence or presence of verapamil (10 μM) for 72 h (MTS assay; n = 4). (G) Intracellular concentrations of QW-5–70 and vincristine in parental SK-N-BE(2)-C and BE2C/VCR cells following 50 nM, 2 h treatment, with or without tariquidar (1 μM), quantified by LC–MS/MS (n = 3). (H) Immunoblot analysis of P-gp expression in PC-3 and PC-3/TxR cells. (I) Cell viability of PC-3/TxR cells treated with QW-5–70 or paclitaxel (0.1 nM–3 μM) in the absence or presence of verapamil (10 μM) for 72 h (MTS assay; n = 4). (J) Intracellular concentrations of QW-5–70 and paclitaxel in PC-3 and PC-3/TxR cells under the same conditions as panel G, quantified by LC–MS/MS (n = 3). (K) Immunoblot analysis of P-gp expression in PC-3/TxR cells following transfection with scrambled control or si-P-gp. GAPDH served as a loading control. (L) Viability of QW-5–70 and paclitaxel in PC-3/TxR, PC-3/TxR-scramble, and PC-3/TxR-si-P-gp cells (MTS assay; n=4).

Techniques: Activity Assay, Expressing, Control, Migration, Western Blot, MTS Assay, Liquid Chromatography with Mass Spectroscopy, Transfection

(A) Cell-cycle distribution of SK-N-BE(2)-C, NB-1691, and PC-3/TxR cells treated with QW-5–70 (2 or 5 nM) for 24 h, analyzed by flow cytometry (n=3). (B, C) Immunoblot analysis of cell-cycle–related proteins (phospho-histone H3 (Ser10), histone H3, cyclin B1, phospho-CDK1 (Thr161), and CDK1) in parental (SK-N-BE(2)-C, NB-1691) and resistant (BE2C/VCR, PC-3/TxR) cells treated with QW-5–70 (2 or 5 nM) for 24 h. (D, E) Immunoblot analysis of apoptosis-related proteins (cCas9, cCas3, PARP, cPARP, p-BCL2 (Ser70), and BCL2) in the same cell lines following 24 h treatment. GAPDH served as a loading control.

Journal: Molecular cancer therapeutics

Article Title: QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp–overexpressing cancer models

doi: 10.1158/1535-7163.MCT-25-1013

Figure Lengend Snippet: (A) Cell-cycle distribution of SK-N-BE(2)-C, NB-1691, and PC-3/TxR cells treated with QW-5–70 (2 or 5 nM) for 24 h, analyzed by flow cytometry (n=3). (B, C) Immunoblot analysis of cell-cycle–related proteins (phospho-histone H3 (Ser10), histone H3, cyclin B1, phospho-CDK1 (Thr161), and CDK1) in parental (SK-N-BE(2)-C, NB-1691) and resistant (BE2C/VCR, PC-3/TxR) cells treated with QW-5–70 (2 or 5 nM) for 24 h. (D, E) Immunoblot analysis of apoptosis-related proteins (cCas9, cCas3, PARP, cPARP, p-BCL2 (Ser70), and BCL2) in the same cell lines following 24 h treatment. GAPDH served as a loading control.

Techniques: Flow Cytometry, Western Blot, Control

(A) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of DFMO (10–1000 μM). Cell viability was assessed using the MTS assay (n=4). (B) CI–Fa analysis of the QW-5–70 and DFMO combination. CI values were calculated using the Chou–Talalay median-effect method for five experimentally tested dose pairs at their corresponding Fa values. CI < 1, CI = 1, and CI > 1 indicate synergistic, additive, and antagonistic interactions, respectively. (C) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of MLN8237 (1–100 nM). Cell viability was assessed using the MTS assay (n=4). (D) SK-N-BE(2)-C cells were treated with 1 nM QW-5–70 in combination with either DFMO (300 μM, top) or MLN8237 (30 nM, bottom) as indicated. Cell lysates were analyzed by immunoblotting for cPARP as a marker of apoptosis, with GAPDH used as a loading control. (E) Representative colony formation images of SK-N-BE(2)-C cells treated with the same combination. Colony formations were quantified and expressed as mean ± SEM relative to vehicle (set to 100%) (n=5).

Journal: Molecular cancer therapeutics

Article Title: QW-5-70 targets the colchicine site and demonstrates antitumor activity in P-gp–overexpressing cancer models

doi: 10.1158/1535-7163.MCT-25-1013

Figure Lengend Snippet: (A) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of DFMO (10–1000 μM). Cell viability was assessed using the MTS assay (n=4). (B) CI–Fa analysis of the QW-5–70 and DFMO combination. CI values were calculated using the Chou–Talalay median-effect method for five experimentally tested dose pairs at their corresponding Fa values. CI < 1, CI = 1, and CI > 1 indicate synergistic, additive, and antagonistic interactions, respectively. (C) SK-N-BE(2)-c cells were treated with five doses of QW-5–70 (0.125 to 2 nM) in combination with five doses of MLN8237 (1–100 nM). Cell viability was assessed using the MTS assay (n=4). (D) SK-N-BE(2)-C cells were treated with 1 nM QW-5–70 in combination with either DFMO (300 μM, top) or MLN8237 (30 nM, bottom) as indicated. Cell lysates were analyzed by immunoblotting for cPARP as a marker of apoptosis, with GAPDH used as a loading control. (E) Representative colony formation images of SK-N-BE(2)-C cells treated with the same combination. Colony formations were quantified and expressed as mean ± SEM relative to vehicle (set to 100%) (n=5).

Techniques: Activity Assay, MTS Assay, Western Blot, Marker, Control

Macrophages cultured with conditioned media from LMO1-overexpressing BE2C cells accelerate tumor-cell migration in vivo (A) Schematic diagram of experimental setup. U937 human monocytes were first differentiated to M0 macrophages with phorbol 12-myristate 13-acetate (PMA) and then cultured in conditioned media (CM) derived from control (“Ctl”) or LMO1-overexpressing (“LMO1”) BE2C cells. Ctl-CM-treated and LMO1-CM-treated U937 cells were labeled with ViaFluor 405 (green-fluorescent) dye. Each group of 405-labeled U937 cells was then combined with mCherry-labeled BE2C cells and co-injected into 2-day-old zebrafish through the perivitelline space (PVS, see diagram for the location of injection). (B–I) Ventral-view (B-E) or lateral-view (F-I) fluorescent images of transplanted zebrafish larvae at 1 day post-injection (dpi, left panels) or 3–4 dpi (right panels) (scale bars, 100 μm). Blue double arrowheads point to the site of injection in panels B-E. Black arrows point to U937 macrophages. Red arrows point to BE2C NB cancer cells. (J) Quantification of transplanted fish with NB cell migration ( n = 55). Migration of NB cells in transplanted recipients was defined as at least one or more mCherry-positive tumor cells located in the anterior regions of the fish, distant from the site of injection (outside of PVS and yolk). ∗∗∗∗ p ≤ 0.0001.

Journal: iScience

Article Title: LMO1 expression in neuroblastoma cells reprograms tumor-associated macrophages to promote metastasis

doi: 10.1016/j.isci.2026.115144

Figure Lengend Snippet: Macrophages cultured with conditioned media from LMO1-overexpressing BE2C cells accelerate tumor-cell migration in vivo (A) Schematic diagram of experimental setup. U937 human monocytes were first differentiated to M0 macrophages with phorbol 12-myristate 13-acetate (PMA) and then cultured in conditioned media (CM) derived from control (“Ctl”) or LMO1-overexpressing (“LMO1”) BE2C cells. Ctl-CM-treated and LMO1-CM-treated U937 cells were labeled with ViaFluor 405 (green-fluorescent) dye. Each group of 405-labeled U937 cells was then combined with mCherry-labeled BE2C cells and co-injected into 2-day-old zebrafish through the perivitelline space (PVS, see diagram for the location of injection). (B–I) Ventral-view (B-E) or lateral-view (F-I) fluorescent images of transplanted zebrafish larvae at 1 day post-injection (dpi, left panels) or 3–4 dpi (right panels) (scale bars, 100 μm). Blue double arrowheads point to the site of injection in panels B-E. Black arrows point to U937 macrophages. Red arrows point to BE2C NB cancer cells. (J) Quantification of transplanted fish with NB cell migration ( n = 55). Migration of NB cells in transplanted recipients was defined as at least one or more mCherry-positive tumor cells located in the anterior regions of the fish, distant from the site of injection (outside of PVS and yolk). ∗∗∗∗ p ≤ 0.0001.

Article Snippet: The human neuroblastoma cell line BE2C (ATCC Cat# CRL-2268, RRID: CVCL_0529) and the U937 (ATCC Cat# CRL-1593.2, RRID:CVCL_0007) human monocytes were obtained from the American Type Culture Collection (ATCC).

Techniques: Cell Culture, Migration, In Vivo, Derivative Assay, Control, Labeling, Injection

Increased levels of metastasis-promoting cytokines are detected in the CM derived from LMO1-overexpressing BE2C cells (A) Cytokine arrays were probed using CM from Ctl BE2C cells (left) and LMO1-overexpressing BE2C cells (right) ( n = 2). Metastasis-promoting cytokines are labeled as follows: red boxes - Angiogenin; orange boxes - angiopoietin-2; green boxes - CD14; light-blue boxes - EGF; dark-blue boxes - Endoglin/CD105; purple boxes - GDF-15; pink boxes - HGF; gray boxes - ICAM-1/CD54; black boxes - CCL2/MCP-1; neon-green boxes - CXCL12/SDF-1 alpha; yellow boxes - VEGFA. (B) Quantitation of relative cytokine levels based on the normalized signal intensity on two independent cytokine array blots ( n = 2). (C) Relative expression of genes (determined by qRT-PCR) encoding the indicated cytokines in Ctl and LMO1-overexpressing BE2C cells ( n = 4). Data in (B) and (C) are presented as mean ± SD. ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001, and ∗∗∗∗ p ≤ 0.0001. ns; not significant.

Journal: iScience

Article Title: LMO1 expression in neuroblastoma cells reprograms tumor-associated macrophages to promote metastasis

doi: 10.1016/j.isci.2026.115144

Figure Lengend Snippet: Increased levels of metastasis-promoting cytokines are detected in the CM derived from LMO1-overexpressing BE2C cells (A) Cytokine arrays were probed using CM from Ctl BE2C cells (left) and LMO1-overexpressing BE2C cells (right) ( n = 2). Metastasis-promoting cytokines are labeled as follows: red boxes - Angiogenin; orange boxes - angiopoietin-2; green boxes - CD14; light-blue boxes - EGF; dark-blue boxes - Endoglin/CD105; purple boxes - GDF-15; pink boxes - HGF; gray boxes - ICAM-1/CD54; black boxes - CCL2/MCP-1; neon-green boxes - CXCL12/SDF-1 alpha; yellow boxes - VEGFA. (B) Quantitation of relative cytokine levels based on the normalized signal intensity on two independent cytokine array blots ( n = 2). (C) Relative expression of genes (determined by qRT-PCR) encoding the indicated cytokines in Ctl and LMO1-overexpressing BE2C cells ( n = 4). Data in (B) and (C) are presented as mean ± SD. ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001, and ∗∗∗∗ p ≤ 0.0001. ns; not significant.

Techniques: Derivative Assay, Labeling, Quantitation Assay, Expressing, Quantitative RT-PCR

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