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ht1080 cells  (ATCC)


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    Structured Review

    ATCC ht1080 cells
    HT enables continuous, label-free monitoring of collagen dynamics through volumetric refractive-index (RI) mapping. a , Time-resolved HT MIPs of type I collagen polymerization showing progressive fibrillar assembly over time. Insets highlight early fibril emergence. Quantification of mean RI change (Δ n ) demonstrates a monotonic increase during gelation, providing a physically calibrated readout of assembly kinetics. b, c , Time-lapse HT imaging of <t>HT1080</t> cells embedded in collagen under pharmacological perturbation (5-min intervals). b , Type I collagen with ROCK inhibitor (Y-27632). c , Type III collagen with MMP inhibitor (GM6001). For each condition, panels show full-field views at representative time points (0, 1, and 2 h), temporally encoded composite images, and zoomed regions highlighting cell-associated matrix remodeling (dashed circles). Drug treatments alter local collagen organization and remodeling dynamics at the single-fiber level compared to controls.
    Ht1080 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 3969 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ht1080 cells/product/ATCC
    Average 98 stars, based on 3969 article reviews
    ht1080 cells - by Bioz Stars, 2026-06
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    Images

    1) Product Images from "Label-free quantitative 3D mapping of collagen architecture by holotomography"

    Article Title: Label-free quantitative 3D mapping of collagen architecture by holotomography

    Journal: bioRxiv

    doi: 10.64898/2026.05.05.722893

    HT enables continuous, label-free monitoring of collagen dynamics through volumetric refractive-index (RI) mapping. a , Time-resolved HT MIPs of type I collagen polymerization showing progressive fibrillar assembly over time. Insets highlight early fibril emergence. Quantification of mean RI change (Δ n ) demonstrates a monotonic increase during gelation, providing a physically calibrated readout of assembly kinetics. b, c , Time-lapse HT imaging of HT1080 cells embedded in collagen under pharmacological perturbation (5-min intervals). b , Type I collagen with ROCK inhibitor (Y-27632). c , Type III collagen with MMP inhibitor (GM6001). For each condition, panels show full-field views at representative time points (0, 1, and 2 h), temporally encoded composite images, and zoomed regions highlighting cell-associated matrix remodeling (dashed circles). Drug treatments alter local collagen organization and remodeling dynamics at the single-fiber level compared to controls.
    Figure Legend Snippet: HT enables continuous, label-free monitoring of collagen dynamics through volumetric refractive-index (RI) mapping. a , Time-resolved HT MIPs of type I collagen polymerization showing progressive fibrillar assembly over time. Insets highlight early fibril emergence. Quantification of mean RI change (Δ n ) demonstrates a monotonic increase during gelation, providing a physically calibrated readout of assembly kinetics. b, c , Time-lapse HT imaging of HT1080 cells embedded in collagen under pharmacological perturbation (5-min intervals). b , Type I collagen with ROCK inhibitor (Y-27632). c , Type III collagen with MMP inhibitor (GM6001). For each condition, panels show full-field views at representative time points (0, 1, and 2 h), temporally encoded composite images, and zoomed regions highlighting cell-associated matrix remodeling (dashed circles). Drug treatments alter local collagen organization and remodeling dynamics at the single-fiber level compared to controls.

    Techniques Used: Refractive Index, Imaging



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    98
    ATCC ht1080 cells
    HT enables continuous, label-free monitoring of collagen dynamics through volumetric refractive-index (RI) mapping. a , Time-resolved HT MIPs of type I collagen polymerization showing progressive fibrillar assembly over time. Insets highlight early fibril emergence. Quantification of mean RI change (Δ n ) demonstrates a monotonic increase during gelation, providing a physically calibrated readout of assembly kinetics. b, c , Time-lapse HT imaging of <t>HT1080</t> cells embedded in collagen under pharmacological perturbation (5-min intervals). b , Type I collagen with ROCK inhibitor (Y-27632). c , Type III collagen with MMP inhibitor (GM6001). For each condition, panels show full-field views at representative time points (0, 1, and 2 h), temporally encoded composite images, and zoomed regions highlighting cell-associated matrix remodeling (dashed circles). Drug treatments alter local collagen organization and remodeling dynamics at the single-fiber level compared to controls.
    Ht1080 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ht1080 cells/product/ATCC
    Average 98 stars, based on 1 article reviews
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    98
    ATCC ht1080 ccl 121 cell lines
    Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in <t>HT1080</t> and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.
    Ht1080 Ccl 121 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ht1080 ccl 121 cell lines/product/ATCC
    Average 98 stars, based on 1 article reviews
    ht1080 ccl 121 cell lines - by Bioz Stars, 2026-06
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    98
    ATCC ht1080 cell lines
    Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in <t>HT1080</t> and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.
    Ht1080 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ht1080 cell lines/product/ATCC
    Average 98 stars, based on 1 article reviews
    ht1080 cell lines - by Bioz Stars, 2026-06
    98/100 stars
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    98
    ATCC fibrosarcoma cell line ht1080
    Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in <t>HT1080</t> and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.
    Fibrosarcoma Cell Line Ht1080, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/fibrosarcoma cell line ht1080/product/ATCC
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    fibrosarcoma cell line ht1080 - by Bioz Stars, 2026-06
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    98
    ATCC ht1080 human fibrosarcoma cell line
    Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in <t>HT1080</t> and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.
    Ht1080 Human Fibrosarcoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ht1080 human fibrosarcoma cell line/product/ATCC
    Average 98 stars, based on 1 article reviews
    ht1080 human fibrosarcoma cell line - by Bioz Stars, 2026-06
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    98
    ATCC human ht1080 cell line
    Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in <t>HT1080</t> and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.
    Human Ht1080 Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human ht1080 cell line/product/ATCC
    Average 98 stars, based on 1 article reviews
    human ht1080 cell line - by Bioz Stars, 2026-06
    98/100 stars
      Buy from Supplier

    Image Search Results


    HT enables continuous, label-free monitoring of collagen dynamics through volumetric refractive-index (RI) mapping. a , Time-resolved HT MIPs of type I collagen polymerization showing progressive fibrillar assembly over time. Insets highlight early fibril emergence. Quantification of mean RI change (Δ n ) demonstrates a monotonic increase during gelation, providing a physically calibrated readout of assembly kinetics. b, c , Time-lapse HT imaging of HT1080 cells embedded in collagen under pharmacological perturbation (5-min intervals). b , Type I collagen with ROCK inhibitor (Y-27632). c , Type III collagen with MMP inhibitor (GM6001). For each condition, panels show full-field views at representative time points (0, 1, and 2 h), temporally encoded composite images, and zoomed regions highlighting cell-associated matrix remodeling (dashed circles). Drug treatments alter local collagen organization and remodeling dynamics at the single-fiber level compared to controls.

    Journal: bioRxiv

    Article Title: Label-free quantitative 3D mapping of collagen architecture by holotomography

    doi: 10.64898/2026.05.05.722893

    Figure Lengend Snippet: HT enables continuous, label-free monitoring of collagen dynamics through volumetric refractive-index (RI) mapping. a , Time-resolved HT MIPs of type I collagen polymerization showing progressive fibrillar assembly over time. Insets highlight early fibril emergence. Quantification of mean RI change (Δ n ) demonstrates a monotonic increase during gelation, providing a physically calibrated readout of assembly kinetics. b, c , Time-lapse HT imaging of HT1080 cells embedded in collagen under pharmacological perturbation (5-min intervals). b , Type I collagen with ROCK inhibitor (Y-27632). c , Type III collagen with MMP inhibitor (GM6001). For each condition, panels show full-field views at representative time points (0, 1, and 2 h), temporally encoded composite images, and zoomed regions highlighting cell-associated matrix remodeling (dashed circles). Drug treatments alter local collagen organization and remodeling dynamics at the single-fiber level compared to controls.

    Article Snippet: HT1080 cells (ATCC, CCL-121) were prepared as a single-cell suspension and mixed with neutralized collagen at 8,000 cells per 60 μL (1.3 × 10 cells/mL) before casting.

    Techniques: Refractive Index, Imaging

    Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in HT1080 and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.

    Journal: Clinical and Translational Medicine

    Article Title: Oncogenic driver and therapeutic target: Prolactin signalling axis in retroperitoneal sarcoma

    doi: 10.1002/ctm2.70669

    Figure Lengend Snippet: Functional characterisation of PRL‐mediated proliferation and chemoresistance in sarcoma models. (A and B) Secretory PRL quantification by ELISA confirming knockdown efficiency in the culture medium, n = 3. (C–F) Growth suppression following PRL depletion: CCK‐8 time‐course assay ( n = 5) and colony formation capacity ( n = 3) in PRL‐knockdown models. (G–J) Recombinant PRL (50 ng/mL)‐induced proliferative enhancement: (G and H) CCK‐8 ( n = 5) and (I and J) colony formation ( n = 3) in HT1080 and SW872 lines. (K–P) PRLR‐dependent proliferation modulation: (K–N) CCK‐8 dose‐response ( n = 5) and (O‐P) colony formation ( n = 3) analysis post‐PRLR perturbation. (Q and R) After treating SW872 and HT1080 cells with PRLR antibody rolinsatamab talirine (20 µg/mL), the effect on cell proliferation was detected by the CCK8 method, with n = 5. (S and T) Xenograft tumourigenesis assay demonstrating impaired SW872 growth with PRL knockdown ( n = 9). (U) A single SW872 clone exhibiting the lowest PRL expression among the pooled PRL‐knockout cells was isolated by limiting dilution cloning, expanded in culture and validated for PRL protein levels via ELISA. (V) Cell proliferation was assessed using the CCK‐8 assay following stable PRL knockout ( n = 5 biological replicates). (W) Bromocriptine‐mediated antiproliferative effects were evaluated in parallel in wild‐type and PRL‐knockout SW872 cell lines using the CCK‐8 assay ( n = 5). (X) In vivo efficacy was determined in a subcutaneous xenograft mouse model, wherein tumour growth derived from wild‐type or PRL‐knockout SW872 cells was monitored following bromocriptine treatment, n = 7. (Y and Z) Chemosensitisation effects: PRL pretreatment (50 ng/mL) enhances cytotoxicity of RG7112/abemaciclib/doxorubicin/gemcitabine, n = 5, RG7112 (10 µM), abemaciclib (5 µM), doxorubicin (2 µM), gemcitabine (10 µM). (a) Western blot analysis was performed to detect MDM2 expression in human adipocytes, liposarcoma cell lines (SW872, 93T449, 94T778), fibrosarcoma cell line HT1080 and clinically isolated liposarcoma cell lines established in our laboratory. (b) Western blot analysis was performed to detect MDM2 in 12 clinical retroperitoneal liposarcoma tissues and its corresponding paracancerous tissues, 6 clinical retroperitoneal fibrosarcoma tissues and corresponding paracancerous tissues. (c) Therapeutic synergy evaluation: bromocriptine combined with RG7112 in WEHI164 fibrosarcoma murine model, RG7112: 100 mg/kg per day, bromocriptine: 10 mg/kg, twice daily, ( n = 6). Data expressed as mean ± SD unless specified; * p < .05, ** p < .01, *** p < .001 by two‐tailed Student's t ‐test; ns: not significant.

    Article Snippet: The SW872 (HTB‐92) and HT1080 (CCL‐121) cell lines were purchased from ATCC.

    Techniques: Functional Assay, Enzyme-linked Immunosorbent Assay, Knockdown, CCK-8 Assay, Recombinant, Expressing, Knock-Out, Isolation, Cloning, In Vivo, Derivative Assay, Western Blot, Two Tailed Test