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ATCC human osa cell lines 143b

CXCL9, -10, or -11 over-secretion from CXCL9 , -10 , or -11 virus-infected <t>OSA</t> cells Production of CXCL9, -10, and -11 by (A) CXCL9 , -10 , and -11 virus-infected <t>143B</t> cells compared with WT 143B cells, (B) CXCL9 , -10 , and -11 virus-infected U2OS cells compared with WT U2OS cells, (C) CXCL9 , -10 , and -11 virus-infected 143B luc cells compared with non-infected 143B luc cells, and (D) CXCL9 , -10 , and -11 virus-infected U2OS luc cells compared with non-infected U2OS luc cells. CM from 143B or U2OS (1.25 × 10 6 cells/mL) were collected after 6 h of incubation and analyzed by the ELISA. Experiments were performed using duplicate samples to obtain an average value. Three to 4 biological repeat experiments were performed. Data are represented as mean ± SD of 3–4 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) secreted significantly increased levels of chemokines compared with their non-infected counterparts. OSA, osteosarcoma; WT, wild-type; luc, luciferase-expressing; CM, conditioned media; ELISA, enzyme-linked immunosorbent assay; SD, standard deviation.

Human Osa Cell Lines 143b, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1412 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma"

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

Journal: Molecular Therapy Oncology

doi: 10.1016/j.omton.2025.201051

CXCL9, -10, or -11 over-secretion from CXCL9 , -10 , or -11 virus-infected OSA cells Production of CXCL9, -10, and -11 by (A) CXCL9 , -10 , and -11 virus-infected 143B cells compared with WT 143B cells, (B) CXCL9 , -10 , and -11 virus-infected U2OS cells compared with WT U2OS cells, (C) CXCL9 , -10 , and -11 virus-infected 143B luc cells compared with non-infected 143B luc cells, and (D) CXCL9 , -10 , and -11 virus-infected U2OS luc cells compared with non-infected U2OS luc cells. CM from 143B or U2OS (1.25 × 10 6 cells/mL) were collected after 6 h of incubation and analyzed by the ELISA. Experiments were performed using duplicate samples to obtain an average value. Three to 4 biological repeat experiments were performed. Data are represented as mean ± SD of 3–4 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) secreted significantly increased levels of chemokines compared with their non-infected counterparts. OSA, osteosarcoma; WT, wild-type; luc, luciferase-expressing; CM, conditioned media; ELISA, enzyme-linked immunosorbent assay; SD, standard deviation.

Figure Legend Snippet: CXCL9, -10, or -11 over-secretion from CXCL9 , -10 , or -11 virus-infected OSA cells Production of CXCL9, -10, and -11 by (A) CXCL9 , -10 , and -11 virus-infected 143B cells compared with WT 143B cells, (B) CXCL9 , -10 , and -11 virus-infected U2OS cells compared with WT U2OS cells, (C) CXCL9 , -10 , and -11 virus-infected 143B luc cells compared with non-infected 143B luc cells, and (D) CXCL9 , -10 , and -11 virus-infected U2OS luc cells compared with non-infected U2OS luc cells. CM from 143B or U2OS (1.25 × 10 6 cells/mL) were collected after 6 h of incubation and analyzed by the ELISA. Experiments were performed using duplicate samples to obtain an average value. Three to 4 biological repeat experiments were performed. Data are represented as mean ± SD of 3–4 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) secreted significantly increased levels of chemokines compared with their non-infected counterparts. OSA, osteosarcoma; WT, wild-type; luc, luciferase-expressing; CM, conditioned media; ELISA, enzyme-linked immunosorbent assay; SD, standard deviation.

Techniques Used: Virus, Infection, Incubation, Enzyme-linked Immunosorbent Assay, Luciferase, Expressing, Standard Deviation

Enhanced in vitro NK migration toward CXCL9 , -10 , or -11 virus-infected OSA CM Transwell migration assay of expanded NK cells toward (A) CM from CXCL9 , -10 , and -11 virus-infected 143B cells relative to WT 143B CM, (B) CM from CXCL9 , -10 , and -11 virus-infected U2OS cells relative to WT U2OS CM, (C) CM from CXCL9 , -10 , and -11 virus-infected 143B luc cells relative to non-infected 143B luc CM, and (D) CM from CXCL9 , -10 , and -11 virus-infected U2OS luc cells relative to non-infected U2OS luc CM. Serum-free media were cultured with 143B or U2OS cells (1.25 × 10 6 cells/mL) for 6 h and transferred to 24-well plates. Expanded NK cells were added at 5 × 10 5 per transwell insert (5-μm pore size filter) and incubated for 2 h. Data are represented as mean ± SD of 3–4 independent biological replicates. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) significantly enhanced NK migration compared with CM from their non-infected counterparts. NK, natural killer; OSA, osteosarcoma; CM, conditioned media; WT, wild-type; luc, luciferase-expressing; SD, standard deviation.

Figure Legend Snippet: Enhanced in vitro NK migration toward CXCL9 , -10 , or -11 virus-infected OSA CM Transwell migration assay of expanded NK cells toward (A) CM from CXCL9 , -10 , and -11 virus-infected 143B cells relative to WT 143B CM, (B) CM from CXCL9 , -10 , and -11 virus-infected U2OS cells relative to WT U2OS CM, (C) CM from CXCL9 , -10 , and -11 virus-infected 143B luc cells relative to non-infected 143B luc CM, and (D) CM from CXCL9 , -10 , and -11 virus-infected U2OS luc cells relative to non-infected U2OS luc CM. Serum-free media were cultured with 143B or U2OS cells (1.25 × 10 6 cells/mL) for 6 h and transferred to 24-well plates. Expanded NK cells were added at 5 × 10 5 per transwell insert (5-μm pore size filter) and incubated for 2 h. Data are represented as mean ± SD of 3–4 independent biological replicates. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) significantly enhanced NK migration compared with CM from their non-infected counterparts. NK, natural killer; OSA, osteosarcoma; CM, conditioned media; WT, wild-type; luc, luciferase-expressing; SD, standard deviation.

Techniques Used: In Vitro, Migration, Virus, Infection, Transwell Migration Assay, Cell Culture, Pore Size, Incubation, Luciferase, Expressing, Standard Deviation

Maintained sensitivity of CXCL9, -10, or -11-secreting OSA cells to NK cell killing NK cytotoxicity against (A) CXCL9 , -10 , and -11 virus-infected and non-infected 143B luc cells, and (B) CXCL9 , -10 , and -11 virus-infected and non-infected U2OS luc cells. Data are represented as mean ± SD of triplicates in a representative experiment. Experiments were repeated 3 times with similar results. ∗∗ p < 0.01 (Student’s t test) in (A). CXCL11 virus-infected 143B luc cells were significantly more sensitive to NK cells than non-infected 143B luc cells at an E:T ratio = 1:10. The other comparison between CXCL9 , -10 , or -11 virus-infected and non-infected OSA cells (143B luc or U2OS luc) at E:T ratios = 1:10 and 1:2 was not statistically significant. OSA, osteosarcoma; NK, natural killer; luc, luciferase-expressing; SD, standard deviation; E:T, effector-to-target.

Figure Legend Snippet: Maintained sensitivity of CXCL9, -10, or -11-secreting OSA cells to NK cell killing NK cytotoxicity against (A) CXCL9 , -10 , and -11 virus-infected and non-infected 143B luc cells, and (B) CXCL9 , -10 , and -11 virus-infected and non-infected U2OS luc cells. Data are represented as mean ± SD of triplicates in a representative experiment. Experiments were repeated 3 times with similar results. ∗∗ p < 0.01 (Student’s t test) in (A). CXCL11 virus-infected 143B luc cells were significantly more sensitive to NK cells than non-infected 143B luc cells at an E:T ratio = 1:10. The other comparison between CXCL9 , -10 , or -11 virus-infected and non-infected OSA cells (143B luc or U2OS luc) at E:T ratios = 1:10 and 1:2 was not statistically significant. OSA, osteosarcoma; NK, natural killer; luc, luciferase-expressing; SD, standard deviation; E:T, effector-to-target.

Techniques Used: Virus, Infection, Comparison, Luciferase, Expressing, Standard Deviation

Increased in vivo NK chemotaxis to CXCL9 , -10 , or -11 virus-infected OSA NSG mice were inoculated s.c. with 2 × 10 6 WT and chemokine (either CXCL9, -10, or -11)-secreting 143B cells in each flank of the same mouse. (A) Xenograft model for migration experiments: five days following tumor inoculation (when tumors were palpable), luciferase-expressing NK cells were injected (i.p. 2.7 × 10 6 ). Mice were imaged using bioluminescent imaging 1–3 h following NK cell injection ( n = 3 mice/group). (B) Example of in vivo imaging of a mouse inoculated with WT (left flank) and chemokine (either CXCL9, -10, or -11)-secreting 143B cells (right flank) treated as described in (A). One of the three representative mice/group is shown. (C) Luminescence from chemokine (either CXCL9, -10, or -11)-secreting tumors relative to WT tumors. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test). CXCL9 , -10 , or -11 virus-infected 143B tumors significantly enhanced NK migration compared with non-infected 143B tumors. The other comparison was not statistically significant. (D) Xenograft model for infiltration experiments: 5–6 days following tumor inoculation, NK cells were injected (i.p. 1.5 × 10 7 ) with NKTR-255 (i.p. 0.3 mg/kg). Tumors were collected 5–7 days after NK cell injection, dissociated, stained with an anti-human CD45 antibody, and analyzed on a flow cytometer ( n = 3 mice/group). (E) Numbers of human CD45 + cells in dissociated CXCL9, -10, or -11-positive tumors relative to WT tumors. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). CXCL9 , -10 , or -11 virus-infected 143B tumors significantly enhanced NK infiltration compared with non-infected 143B tumors. CXCL10 virus-infected 143B tumors significantly enhanced NK infiltration compared with CXCL9 or -11 virus-infected 143B tumors. The comparison between CXCL9 virus-infected and CXCL11 virus-infected 143B tumors was not statistically significant. NK, natural killer; OSA, osteosarcoma; NSG, NOD/SCID/gamma −/− ; s.c., subcutaneously; WT, wild-type; i.p., intraperitoneally; SD, standard deviation.

Figure Legend Snippet: Increased in vivo NK chemotaxis to CXCL9 , -10 , or -11 virus-infected OSA NSG mice were inoculated s.c. with 2 × 10 6 WT and chemokine (either CXCL9, -10, or -11)-secreting 143B cells in each flank of the same mouse. (A) Xenograft model for migration experiments: five days following tumor inoculation (when tumors were palpable), luciferase-expressing NK cells were injected (i.p. 2.7 × 10 6 ). Mice were imaged using bioluminescent imaging 1–3 h following NK cell injection ( n = 3 mice/group). (B) Example of in vivo imaging of a mouse inoculated with WT (left flank) and chemokine (either CXCL9, -10, or -11)-secreting 143B cells (right flank) treated as described in (A). One of the three representative mice/group is shown. (C) Luminescence from chemokine (either CXCL9, -10, or -11)-secreting tumors relative to WT tumors. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test). CXCL9 , -10 , or -11 virus-infected 143B tumors significantly enhanced NK migration compared with non-infected 143B tumors. The other comparison was not statistically significant. (D) Xenograft model for infiltration experiments: 5–6 days following tumor inoculation, NK cells were injected (i.p. 1.5 × 10 7 ) with NKTR-255 (i.p. 0.3 mg/kg). Tumors were collected 5–7 days after NK cell injection, dissociated, stained with an anti-human CD45 antibody, and analyzed on a flow cytometer ( n = 3 mice/group). (E) Numbers of human CD45 + cells in dissociated CXCL9, -10, or -11-positive tumors relative to WT tumors. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). CXCL9 , -10 , or -11 virus-infected 143B tumors significantly enhanced NK infiltration compared with non-infected 143B tumors. CXCL10 virus-infected 143B tumors significantly enhanced NK infiltration compared with CXCL9 or -11 virus-infected 143B tumors. The comparison between CXCL9 virus-infected and CXCL11 virus-infected 143B tumors was not statistically significant. NK, natural killer; OSA, osteosarcoma; NSG, NOD/SCID/gamma −/− ; s.c., subcutaneously; WT, wild-type; i.p., intraperitoneally; SD, standard deviation.

Techniques Used: In Vivo, Chemotaxis Assay, Virus, Infection, Migration, Luciferase, Expressing, Injection, Imaging, In Vivo Imaging, Comparison, Staining, Flow Cytometry, Standard Deviation

Decreased tumor burden and prolonged survival in mice bearing CXCL10 + tumors following adoptive transfer of NK cells with NKTR-255 (A) NK cytotoxicity against CXCL10 virus-infected and non-infected 143B luc cells with or without NKTR-255 (40 ng/mL). Data are represented as mean ± SD of the triplicates in a representative experiment. Experiments were repeated 3 times with similar results. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test). NKTR-255 significantly enhanced NK cytotoxicity against both CXCL10 virus-infected and non-infected 143B luc cells compared with NK cells alone at E:T ratios = 1:5 and 1:2. (B) Growth curve of WT and CXCL10 + 143B cells. Data are represented as mean ± SD of 3 independent biological replicates. The comparison between WT and CXCL10 + 143B cells was not statistically significant (Student’s t test). (C) Xenograft model for tumor progression and survival analysis: NSG mice were inoculated s.c. with 5 × 10 5 WT or CXCL10 + 143B cells in individual mice. Mice were divided into 4 treatment groups: PBS, NKTR-255, NK, and NK+NKTR-255. NK cell injections (i.p. 1 × 10 7 ) and NKTR-255 injections (i.p. 0.3 mg/kg) started 1 day following tumor inoculation. A total of six infusions of NK cells were administered every 7 days. A total of two infusions of NKTR-255 were administered every 3 weeks ( n = 8–10 mice/group). (D) Tumor burden measured by a digital caliper 8–29 days after tumor inoculation in mice bearing either WT or CXCL10 + tumors treated with PBS, NKTR-255 alone, NK cells alone, or the combinatorial therapy of NK cells and NKTR-255. Tumor volume at the time of death was used for subsequent tumor volume of mice that died before 29 days post tumor inoculation. n = 8–10 mice/group. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗∗ p < 0.001 (ANOVA with post hoc Bonferroni test). NK significantly reduced CXCL10 + tumor burden compared with WT tumor burden. NK significantly reduced CXCL10 + tumor burden compared with PBS. NK+NKTR-255 significantly reduced CXCL10 + tumor burden compared with WT tumor burden. NK+NKTR-255 significantly reduced CXCL10 + tumor burden compared with PBS, NKTR-255, or NK. The comparison of WT and CXCL10 + tumor burden treated with PBS or NKTR-255 was not statistically significant. The comparison of WT tumor burden among the treatment groups was not statistically significant. (E) Survival of mice bearing either WT or CXCL10 + 143B tumors treated with PBS, NKTR-255 alone, NK cells alone, or the combinatorial therapy of NK cells and NKTR-255. n = 8–10 mice/group. ∗ p < 0.05, ∗∗ p < 0.01 (log rank test). NK+NKTR-255 significantly extended survival of mice bearing CXCL10 + tumors compared with mice bearing WT tumors. NK+NKTR255 significantly extended survival of mice bearing CXCL10 + tumors compared with PBS or NKTR-255 alone. The comparison of survival of mice bearing WT or CXCL10 + tumors treated with PBS or NKTR-255 was not statistically significant. The comparison of survival of mice bearing WT tumors among the treatment groups was not statistically significant. NK, natural killer; luc, luciferase-expressing; SD, standard deviation; WT, wild-type; NSG, NOD/SCID/gamma −/− ; s.c.; subcutaneously; PBS, phosphate buffer solution; i.p., intraperitoneally; ANOVA, analysis of variance.

Figure Legend Snippet: Decreased tumor burden and prolonged survival in mice bearing CXCL10 + tumors following adoptive transfer of NK cells with NKTR-255 (A) NK cytotoxicity against CXCL10 virus-infected and non-infected 143B luc cells with or without NKTR-255 (40 ng/mL). Data are represented as mean ± SD of the triplicates in a representative experiment. Experiments were repeated 3 times with similar results. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test). NKTR-255 significantly enhanced NK cytotoxicity against both CXCL10 virus-infected and non-infected 143B luc cells compared with NK cells alone at E:T ratios = 1:5 and 1:2. (B) Growth curve of WT and CXCL10 + 143B cells. Data are represented as mean ± SD of 3 independent biological replicates. The comparison between WT and CXCL10 + 143B cells was not statistically significant (Student’s t test). (C) Xenograft model for tumor progression and survival analysis: NSG mice were inoculated s.c. with 5 × 10 5 WT or CXCL10 + 143B cells in individual mice. Mice were divided into 4 treatment groups: PBS, NKTR-255, NK, and NK+NKTR-255. NK cell injections (i.p. 1 × 10 7 ) and NKTR-255 injections (i.p. 0.3 mg/kg) started 1 day following tumor inoculation. A total of six infusions of NK cells were administered every 7 days. A total of two infusions of NKTR-255 were administered every 3 weeks ( n = 8–10 mice/group). (D) Tumor burden measured by a digital caliper 8–29 days after tumor inoculation in mice bearing either WT or CXCL10 + tumors treated with PBS, NKTR-255 alone, NK cells alone, or the combinatorial therapy of NK cells and NKTR-255. Tumor volume at the time of death was used for subsequent tumor volume of mice that died before 29 days post tumor inoculation. n = 8–10 mice/group. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗∗ p < 0.001 (ANOVA with post hoc Bonferroni test). NK significantly reduced CXCL10 + tumor burden compared with WT tumor burden. NK significantly reduced CXCL10 + tumor burden compared with PBS. NK+NKTR-255 significantly reduced CXCL10 + tumor burden compared with WT tumor burden. NK+NKTR-255 significantly reduced CXCL10 + tumor burden compared with PBS, NKTR-255, or NK. The comparison of WT and CXCL10 + tumor burden treated with PBS or NKTR-255 was not statistically significant. The comparison of WT tumor burden among the treatment groups was not statistically significant. (E) Survival of mice bearing either WT or CXCL10 + 143B tumors treated with PBS, NKTR-255 alone, NK cells alone, or the combinatorial therapy of NK cells and NKTR-255. n = 8–10 mice/group. ∗ p < 0.05, ∗∗ p < 0.01 (log rank test). NK+NKTR-255 significantly extended survival of mice bearing CXCL10 + tumors compared with mice bearing WT tumors. NK+NKTR255 significantly extended survival of mice bearing CXCL10 + tumors compared with PBS or NKTR-255 alone. The comparison of survival of mice bearing WT or CXCL10 + tumors treated with PBS or NKTR-255 was not statistically significant. The comparison of survival of mice bearing WT tumors among the treatment groups was not statistically significant. NK, natural killer; luc, luciferase-expressing; SD, standard deviation; WT, wild-type; NSG, NOD/SCID/gamma −/− ; s.c.; subcutaneously; PBS, phosphate buffer solution; i.p., intraperitoneally; ANOVA, analysis of variance.

Techniques Used: Adoptive Transfer Assay, Virus, Infection, Comparison, Luciferase, Expressing, Standard Deviation

Upregulation of apoptosis and TGF-β signaling following treatment with NK cells and NKTR-255 (A) Xenograft model for analysis of response and resistance mechanisms: NSG mice were inoculated s.c. with 5 × 10 5 WT and CXCL10 + 143B cells in each flank of the same mouse. Mice were divided into 2 treatment groups: PBS and NK+NKTR-255. NK cell injections (i.p. 1.5 × 10 7 ) and NKTR-255 injections (i.p. 0.3 mg/kg) started 1 day following tumor inoculation. A total of three infusions of NK cells were administered every 7 days. Tumors were collected 21–23 days after tumor injection, dissociated, and analyzed by scRNA-seq ( n = 1 mouse/group) and mass cytometry ( n = 3 mice/group) following red blood cell removal and dead cell removal. (B) Percentage of total leukocytes, neutrophils, and macrophages (identified by scRNA-seq as described in ) in mouse cells infiltrating into each tumor. (C) Percentage of mouse CD45.1 + cells (detected by mass cytometry) in total live cells in each tumor. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). PBS-treated CXCL10 + tumors significantly enhanced mouse leukocyte infiltration compared with PBS-treated WT tumors. NK+NKTR-255-treated CXCL10 + tumors significantly enhanced mouse leukocyte infiltration compared with NK+NKTR-255-treated WT tumors. (D) Mean expression of IFIT2 by pooled analysis of scRNA-seq data on OSA cells in each tumor. (E) Violin plot detailing the percentage of mitochondrial genes in cells that passed QC thresholds (percentage of mitochondrial genes <20%, nCount_RNA <25,000, nFeature_RNA >200 and <5,000) from each tumor. Box represents median. (F) GSEA bar chart showing enrichment scores for the hallmark pathways that were different between CXCL10 + tumors with and without treatment with NK cells and NKTR-255. Pathways upregulated in the CXCL10 + tumor treated with NK cells and NKTR-255 were shown in orange. Pathways downregulated in the CXCL10 + tumor treated with NK cells and NKTR-255 were shown in blue. Pathways indicated by arrowhead (◄) were related to cell death. See also . (G) Mass cytometry plot showing pRb vs. cPARP channel of OSA cells (hCD45 − mCD45.1 − pRb high GAPDH high ) in a CXCL10 + tumor with or without treatment with NK cells and NKTR-255. One of the three representative plots/treatment group is shown. (H) Percentage of cPARP + OSA cells (hCD45 − mCD45.1 − pRb high GAPDH high ) in CXCL10 + tumors with or without treatment with NK cells and NKTR-255. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). NK+NKTR-255 significantly increased expression of cPARP in CXCL10 + tumors compared with PBS. (I) GSEA enrichment plot on mouse macrophages identified by scRNA-seq. Signaling by TGF-β receptor complex was the top pathway positively enriched in the NK+NKTR-255-treated CXCL10 + tumor compared with the PBS-treated CXCL10 + tumor. See also . NK_CXCL, NK+NKTR-255-treated CXCL10 + OSA; NK_WT, NK+NKTR-255-treated WT OSA; PBS_CXCL, PBS-treated CXCL10 + OSA; PBS_WT, PBS-treated WT OSA; NK, natural killer; OSA, osteosarcoma; WT, wild-type; PBS, phosphate buffer solution; NSG, NOD/SCID/gamma −/− ; s.c., subcutaneously; i.p., intraperitoneally; scRNA-seq, single-cell RNA sequencing; SD, standard deviation; QC, quality control; GSEA, gene set enrichment analysis.

Figure Legend Snippet: Upregulation of apoptosis and TGF-β signaling following treatment with NK cells and NKTR-255 (A) Xenograft model for analysis of response and resistance mechanisms: NSG mice were inoculated s.c. with 5 × 10 5 WT and CXCL10 + 143B cells in each flank of the same mouse. Mice were divided into 2 treatment groups: PBS and NK+NKTR-255. NK cell injections (i.p. 1.5 × 10 7 ) and NKTR-255 injections (i.p. 0.3 mg/kg) started 1 day following tumor inoculation. A total of three infusions of NK cells were administered every 7 days. Tumors were collected 21–23 days after tumor injection, dissociated, and analyzed by scRNA-seq ( n = 1 mouse/group) and mass cytometry ( n = 3 mice/group) following red blood cell removal and dead cell removal. (B) Percentage of total leukocytes, neutrophils, and macrophages (identified by scRNA-seq as described in ) in mouse cells infiltrating into each tumor. (C) Percentage of mouse CD45.1 + cells (detected by mass cytometry) in total live cells in each tumor. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). PBS-treated CXCL10 + tumors significantly enhanced mouse leukocyte infiltration compared with PBS-treated WT tumors. NK+NKTR-255-treated CXCL10 + tumors significantly enhanced mouse leukocyte infiltration compared with NK+NKTR-255-treated WT tumors. (D) Mean expression of IFIT2 by pooled analysis of scRNA-seq data on OSA cells in each tumor. (E) Violin plot detailing the percentage of mitochondrial genes in cells that passed QC thresholds (percentage of mitochondrial genes <20%, nCount_RNA <25,000, nFeature_RNA >200 and <5,000) from each tumor. Box represents median. (F) GSEA bar chart showing enrichment scores for the hallmark pathways that were different between CXCL10 + tumors with and without treatment with NK cells and NKTR-255. Pathways upregulated in the CXCL10 + tumor treated with NK cells and NKTR-255 were shown in orange. Pathways downregulated in the CXCL10 + tumor treated with NK cells and NKTR-255 were shown in blue. Pathways indicated by arrowhead (◄) were related to cell death. See also . (G) Mass cytometry plot showing pRb vs. cPARP channel of OSA cells (hCD45 − mCD45.1 − pRb high GAPDH high ) in a CXCL10 + tumor with or without treatment with NK cells and NKTR-255. One of the three representative plots/treatment group is shown. (H) Percentage of cPARP + OSA cells (hCD45 − mCD45.1 − pRb high GAPDH high ) in CXCL10 + tumors with or without treatment with NK cells and NKTR-255. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). NK+NKTR-255 significantly increased expression of cPARP in CXCL10 + tumors compared with PBS. (I) GSEA enrichment plot on mouse macrophages identified by scRNA-seq. Signaling by TGF-β receptor complex was the top pathway positively enriched in the NK+NKTR-255-treated CXCL10 + tumor compared with the PBS-treated CXCL10 + tumor. See also . NK_CXCL, NK+NKTR-255-treated CXCL10 + OSA; NK_WT, NK+NKTR-255-treated WT OSA; PBS_CXCL, PBS-treated CXCL10 + OSA; PBS_WT, PBS-treated WT OSA; NK, natural killer; OSA, osteosarcoma; WT, wild-type; PBS, phosphate buffer solution; NSG, NOD/SCID/gamma −/− ; s.c., subcutaneously; i.p., intraperitoneally; scRNA-seq, single-cell RNA sequencing; SD, standard deviation; QC, quality control; GSEA, gene set enrichment analysis.

Techniques Used: Injection, Mass Cytometry, Expressing, RNA Sequencing, Standard Deviation, Control

Image Search Results

Journal: Molecular Therapy Oncology

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

doi: 10.1016/j.omton.2025.201051

Figure Lengend Snippet: CXCL9, -10, or -11 over-secretion from CXCL9 , -10 , or -11 virus-infected OSA cells Production of CXCL9, -10, and -11 by (A) CXCL9 , -10 , and -11 virus-infected 143B cells compared with WT 143B cells, (B) CXCL9 , -10 , and -11 virus-infected U2OS cells compared with WT U2OS cells, (C) CXCL9 , -10 , and -11 virus-infected 143B luc cells compared with non-infected 143B luc cells, and (D) CXCL9 , -10 , and -11 virus-infected U2OS luc cells compared with non-infected U2OS luc cells. CM from 143B or U2OS (1.25 × 10 6 cells/mL) were collected after 6 h of incubation and analyzed by the ELISA. Experiments were performed using duplicate samples to obtain an average value. Three to 4 biological repeat experiments were performed. Data are represented as mean ± SD of 3–4 independent experiments. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) secreted significantly increased levels of chemokines compared with their non-infected counterparts. OSA, osteosarcoma; WT, wild-type; luc, luciferase-expressing; CM, conditioned media; ELISA, enzyme-linked immunosorbent assay; SD, standard deviation.

Article Snippet: The human OSA cell lines 143B (RRID: CVCL_2270) and U2OS (RRID: CVCL_0042) were obtained from American Type Culture Collection ( https://www.atcc.org ).

Techniques: Virus, Infection, Incubation, Enzyme-linked Immunosorbent Assay, Luciferase, Expressing, Standard Deviation

Journal: Molecular Therapy Oncology

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

doi: 10.1016/j.omton.2025.201051

Figure Lengend Snippet: Enhanced in vitro NK migration toward CXCL9 , -10 , or -11 virus-infected OSA CM Transwell migration assay of expanded NK cells toward (A) CM from CXCL9 , -10 , and -11 virus-infected 143B cells relative to WT 143B CM, (B) CM from CXCL9 , -10 , and -11 virus-infected U2OS cells relative to WT U2OS CM, (C) CM from CXCL9 , -10 , and -11 virus-infected 143B luc cells relative to non-infected 143B luc CM, and (D) CM from CXCL9 , -10 , and -11 virus-infected U2OS luc cells relative to non-infected U2OS luc CM. Serum-free media were cultured with 143B or U2OS cells (1.25 × 10 6 cells/mL) for 6 h and transferred to 24-well plates. Expanded NK cells were added at 5 × 10 5 per transwell insert (5-μm pore size filter) and incubated for 2 h. Data are represented as mean ± SD of 3–4 independent biological replicates. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 (Student’s t test) in (A), (B), (C), and (D). CM from CXCL9 , -10 , or -11 virus-infected OSA cells (143B, U2OS, 143B luc, or U2OS luc) significantly enhanced NK migration compared with CM from their non-infected counterparts. NK, natural killer; OSA, osteosarcoma; CM, conditioned media; WT, wild-type; luc, luciferase-expressing; SD, standard deviation.

Article Snippet: The human OSA cell lines 143B (RRID: CVCL_2270) and U2OS (RRID: CVCL_0042) were obtained from American Type Culture Collection ( https://www.atcc.org ).

Techniques: In Vitro, Migration, Virus, Infection, Transwell Migration Assay, Cell Culture, Pore Size, Incubation, Luciferase, Expressing, Standard Deviation

Journal: Molecular Therapy Oncology

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

doi: 10.1016/j.omton.2025.201051

Figure Lengend Snippet: Maintained sensitivity of CXCL9, -10, or -11-secreting OSA cells to NK cell killing NK cytotoxicity against (A) CXCL9 , -10 , and -11 virus-infected and non-infected 143B luc cells, and (B) CXCL9 , -10 , and -11 virus-infected and non-infected U2OS luc cells. Data are represented as mean ± SD of triplicates in a representative experiment. Experiments were repeated 3 times with similar results. ∗∗ p < 0.01 (Student’s t test) in (A). CXCL11 virus-infected 143B luc cells were significantly more sensitive to NK cells than non-infected 143B luc cells at an E:T ratio = 1:10. The other comparison between CXCL9 , -10 , or -11 virus-infected and non-infected OSA cells (143B luc or U2OS luc) at E:T ratios = 1:10 and 1:2 was not statistically significant. OSA, osteosarcoma; NK, natural killer; luc, luciferase-expressing; SD, standard deviation; E:T, effector-to-target.

Article Snippet: The human OSA cell lines 143B (RRID: CVCL_2270) and U2OS (RRID: CVCL_0042) were obtained from American Type Culture Collection ( https://www.atcc.org ).

Techniques: Virus, Infection, Comparison, Luciferase, Expressing, Standard Deviation

Journal: Molecular Therapy Oncology

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

doi: 10.1016/j.omton.2025.201051

Figure Lengend Snippet: Increased in vivo NK chemotaxis to CXCL9 , -10 , or -11 virus-infected OSA NSG mice were inoculated s.c. with 2 × 10 6 WT and chemokine (either CXCL9, -10, or -11)-secreting 143B cells in each flank of the same mouse. (A) Xenograft model for migration experiments: five days following tumor inoculation (when tumors were palpable), luciferase-expressing NK cells were injected (i.p. 2.7 × 10 6 ). Mice were imaged using bioluminescent imaging 1–3 h following NK cell injection ( n = 3 mice/group). (B) Example of in vivo imaging of a mouse inoculated with WT (left flank) and chemokine (either CXCL9, -10, or -11)-secreting 143B cells (right flank) treated as described in (A). One of the three representative mice/group is shown. (C) Luminescence from chemokine (either CXCL9, -10, or -11)-secreting tumors relative to WT tumors. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test). CXCL9 , -10 , or -11 virus-infected 143B tumors significantly enhanced NK migration compared with non-infected 143B tumors. The other comparison was not statistically significant. (D) Xenograft model for infiltration experiments: 5–6 days following tumor inoculation, NK cells were injected (i.p. 1.5 × 10 7 ) with NKTR-255 (i.p. 0.3 mg/kg). Tumors were collected 5–7 days after NK cell injection, dissociated, stained with an anti-human CD45 antibody, and analyzed on a flow cytometer ( n = 3 mice/group). (E) Numbers of human CD45 + cells in dissociated CXCL9, -10, or -11-positive tumors relative to WT tumors. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). CXCL9 , -10 , or -11 virus-infected 143B tumors significantly enhanced NK infiltration compared with non-infected 143B tumors. CXCL10 virus-infected 143B tumors significantly enhanced NK infiltration compared with CXCL9 or -11 virus-infected 143B tumors. The comparison between CXCL9 virus-infected and CXCL11 virus-infected 143B tumors was not statistically significant. NK, natural killer; OSA, osteosarcoma; NSG, NOD/SCID/gamma −/− ; s.c., subcutaneously; WT, wild-type; i.p., intraperitoneally; SD, standard deviation.

Article Snippet: The human OSA cell lines 143B (RRID: CVCL_2270) and U2OS (RRID: CVCL_0042) were obtained from American Type Culture Collection ( https://www.atcc.org ).

Techniques: In Vivo, Chemotaxis Assay, Virus, Infection, Migration, Luciferase, Expressing, Injection, Imaging, In Vivo Imaging, Comparison, Staining, Flow Cytometry, Standard Deviation

Journal: Molecular Therapy Oncology

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

doi: 10.1016/j.omton.2025.201051

Figure Lengend Snippet: Decreased tumor burden and prolonged survival in mice bearing CXCL10 + tumors following adoptive transfer of NK cells with NKTR-255 (A) NK cytotoxicity against CXCL10 virus-infected and non-infected 143B luc cells with or without NKTR-255 (40 ng/mL). Data are represented as mean ± SD of the triplicates in a representative experiment. Experiments were repeated 3 times with similar results. ∗ p < 0.05, ∗∗ p < 0.01 (Student’s t test). NKTR-255 significantly enhanced NK cytotoxicity against both CXCL10 virus-infected and non-infected 143B luc cells compared with NK cells alone at E:T ratios = 1:5 and 1:2. (B) Growth curve of WT and CXCL10 + 143B cells. Data are represented as mean ± SD of 3 independent biological replicates. The comparison between WT and CXCL10 + 143B cells was not statistically significant (Student’s t test). (C) Xenograft model for tumor progression and survival analysis: NSG mice were inoculated s.c. with 5 × 10 5 WT or CXCL10 + 143B cells in individual mice. Mice were divided into 4 treatment groups: PBS, NKTR-255, NK, and NK+NKTR-255. NK cell injections (i.p. 1 × 10 7 ) and NKTR-255 injections (i.p. 0.3 mg/kg) started 1 day following tumor inoculation. A total of six infusions of NK cells were administered every 7 days. A total of two infusions of NKTR-255 were administered every 3 weeks ( n = 8–10 mice/group). (D) Tumor burden measured by a digital caliper 8–29 days after tumor inoculation in mice bearing either WT or CXCL10 + tumors treated with PBS, NKTR-255 alone, NK cells alone, or the combinatorial therapy of NK cells and NKTR-255. Tumor volume at the time of death was used for subsequent tumor volume of mice that died before 29 days post tumor inoculation. n = 8–10 mice/group. Data are represented as mean ± SD. ∗ p < 0.05, ∗∗∗ p < 0.001 (ANOVA with post hoc Bonferroni test). NK significantly reduced CXCL10 + tumor burden compared with WT tumor burden. NK significantly reduced CXCL10 + tumor burden compared with PBS. NK+NKTR-255 significantly reduced CXCL10 + tumor burden compared with WT tumor burden. NK+NKTR-255 significantly reduced CXCL10 + tumor burden compared with PBS, NKTR-255, or NK. The comparison of WT and CXCL10 + tumor burden treated with PBS or NKTR-255 was not statistically significant. The comparison of WT tumor burden among the treatment groups was not statistically significant. (E) Survival of mice bearing either WT or CXCL10 + 143B tumors treated with PBS, NKTR-255 alone, NK cells alone, or the combinatorial therapy of NK cells and NKTR-255. n = 8–10 mice/group. ∗ p < 0.05, ∗∗ p < 0.01 (log rank test). NK+NKTR-255 significantly extended survival of mice bearing CXCL10 + tumors compared with mice bearing WT tumors. NK+NKTR255 significantly extended survival of mice bearing CXCL10 + tumors compared with PBS or NKTR-255 alone. The comparison of survival of mice bearing WT or CXCL10 + tumors treated with PBS or NKTR-255 was not statistically significant. The comparison of survival of mice bearing WT tumors among the treatment groups was not statistically significant. NK, natural killer; luc, luciferase-expressing; SD, standard deviation; WT, wild-type; NSG, NOD/SCID/gamma −/− ; s.c.; subcutaneously; PBS, phosphate buffer solution; i.p., intraperitoneally; ANOVA, analysis of variance.

Article Snippet: The human OSA cell lines 143B (RRID: CVCL_2270) and U2OS (RRID: CVCL_0042) were obtained from American Type Culture Collection ( https://www.atcc.org ).

Techniques: Adoptive Transfer Assay, Virus, Infection, Comparison, Luciferase, Expressing, Standard Deviation

Journal: Molecular Therapy Oncology

Article Title: CXCL10-induced chemotaxis of ex vivo -expanded natural killer cells combined with NKTR-255 enhances anti-tumor efficacy in osteosarcoma

doi: 10.1016/j.omton.2025.201051

Figure Lengend Snippet: Upregulation of apoptosis and TGF-β signaling following treatment with NK cells and NKTR-255 (A) Xenograft model for analysis of response and resistance mechanisms: NSG mice were inoculated s.c. with 5 × 10 5 WT and CXCL10 + 143B cells in each flank of the same mouse. Mice were divided into 2 treatment groups: PBS and NK+NKTR-255. NK cell injections (i.p. 1.5 × 10 7 ) and NKTR-255 injections (i.p. 0.3 mg/kg) started 1 day following tumor inoculation. A total of three infusions of NK cells were administered every 7 days. Tumors were collected 21–23 days after tumor injection, dissociated, and analyzed by scRNA-seq ( n = 1 mouse/group) and mass cytometry ( n = 3 mice/group) following red blood cell removal and dead cell removal. (B) Percentage of total leukocytes, neutrophils, and macrophages (identified by scRNA-seq as described in ) in mouse cells infiltrating into each tumor. (C) Percentage of mouse CD45.1 + cells (detected by mass cytometry) in total live cells in each tumor. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). PBS-treated CXCL10 + tumors significantly enhanced mouse leukocyte infiltration compared with PBS-treated WT tumors. NK+NKTR-255-treated CXCL10 + tumors significantly enhanced mouse leukocyte infiltration compared with NK+NKTR-255-treated WT tumors. (D) Mean expression of IFIT2 by pooled analysis of scRNA-seq data on OSA cells in each tumor. (E) Violin plot detailing the percentage of mitochondrial genes in cells that passed QC thresholds (percentage of mitochondrial genes <20%, nCount_RNA <25,000, nFeature_RNA >200 and <5,000) from each tumor. Box represents median. (F) GSEA bar chart showing enrichment scores for the hallmark pathways that were different between CXCL10 + tumors with and without treatment with NK cells and NKTR-255. Pathways upregulated in the CXCL10 + tumor treated with NK cells and NKTR-255 were shown in orange. Pathways downregulated in the CXCL10 + tumor treated with NK cells and NKTR-255 were shown in blue. Pathways indicated by arrowhead (◄) were related to cell death. See also . (G) Mass cytometry plot showing pRb vs. cPARP channel of OSA cells (hCD45 − mCD45.1 − pRb high GAPDH high ) in a CXCL10 + tumor with or without treatment with NK cells and NKTR-255. One of the three representative plots/treatment group is shown. (H) Percentage of cPARP + OSA cells (hCD45 − mCD45.1 − pRb high GAPDH high ) in CXCL10 + tumors with or without treatment with NK cells and NKTR-255. Data are represented as mean ± SD. ∗ p < 0.05 (Student’s t test). NK+NKTR-255 significantly increased expression of cPARP in CXCL10 + tumors compared with PBS. (I) GSEA enrichment plot on mouse macrophages identified by scRNA-seq. Signaling by TGF-β receptor complex was the top pathway positively enriched in the NK+NKTR-255-treated CXCL10 + tumor compared with the PBS-treated CXCL10 + tumor. See also . NK_CXCL, NK+NKTR-255-treated CXCL10 + OSA; NK_WT, NK+NKTR-255-treated WT OSA; PBS_CXCL, PBS-treated CXCL10 + OSA; PBS_WT, PBS-treated WT OSA; NK, natural killer; OSA, osteosarcoma; WT, wild-type; PBS, phosphate buffer solution; NSG, NOD/SCID/gamma −/− ; s.c., subcutaneously; i.p., intraperitoneally; scRNA-seq, single-cell RNA sequencing; SD, standard deviation; QC, quality control; GSEA, gene set enrichment analysis.

Article Snippet: The human OSA cell lines 143B (RRID: CVCL_2270) and U2OS (RRID: CVCL_0042) were obtained from American Type Culture Collection ( https://www.atcc.org ).

Techniques: Injection, Mass Cytometry, Expressing, RNA Sequencing, Standard Deviation, Control

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