exosome treated group Search Results


exosomal hmgb1  (Exosome Diagnostics)
86
Exosome Diagnostics exosomal hmgb1
Exosomal <t>HMGB1</t> predicts poor prognosis in NSCLC. (A) A total of 80 NSCLC patients were categorised into metastasis ( n = 32) and nonmetastasis ( n = 48) groups. Blood‐derived exosomes were isolated, quantified and subjected to protein extraction for further analysis. A schematic workflow is presented. (B) Quantification of circulating exosome numbers in blood samples from the metastasis and nonmetastasis NSCLC patient groups. (C) Potential secretory protein factors within exosomes, particularly those implicated in lung cancer progression, were analysed. HMGB1 and Galectin‐9 was identified as a key candidate. A schematic diagram and quantification of exosomal TGF‐β, HMGB1, Galectin‐9 and MMP9 are shown. (D) Quantification of exosomal HMGB1 and galectin‐9 levels in the metastasis and nonmetastasis NSCLC groups. (E) Immunohistochemical (IHC) staining of HMGB1 in tumour tissues from patients with and without metastasis, followed by statistical analysis. (F) Correlation analysis between circulating exosomal HMGB1 concentrations and HMGB1 expression in tumour tissues from all 80 NSCLC patients. (G) Kaplan–Meier survival analysis based on HMGB1 expression in 558 NSCLC patients from the TCGA database. (H) Correlation analysis between HMGB1 expression and stemness scores across different cancer types using the Sanger database. (I) Heatmap showing expression of core stemness‐related genes (CD133, ALDH1, Nanog, Oct4, SOX2, KLF4, CD44) in tumour tissues from 12 NSCLC patients, stratified into HMGB1 low and HMGB1 high groups.
Exosomal Hmgb1, supplied by Exosome Diagnostics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/exosomal hmgb1/product/Exosome Diagnostics
Average 86 stars, based on 1 article reviews
exosomal hmgb1 - by Bioz Stars, 2026-06
86/100 stars
  Buy from Supplier
exosome treated groups  (Exosome Diagnostics)
86
Exosome Diagnostics exosome treated groups
CSCs-, HT-29- and Caco-2-derived exosomes decreased the proliferation of Caco-2 and HT-29 cells. A Comparative analysis of Caco-2 cell proliferation after treatment with exosomes at different time intervals (24, 48, and 72 h) ( n = 3). As observed in the <t>graph,</t> <t>exosome-treated</t> groups (CSCs-, HT-29-, and Caco-2-derived exosomes) showed decreased cell proliferation compared to untreated groups and PBS. Cell proliferation was higher in cells treated with CSCs- derived exosomes compared to cells treated with HT-29-, and Caco-2-derived exosomes. B Comparative analysis of HT-29 cell proliferation after treatment with exosomes at 48 h ( n = 3). Exosome-treated groups showed a significant decrease in cell proliferation compared to untreated and PBS-treated groups. Following Bonferroni correction, the difference in cell proliferation was statistically significant ( p < 0.05) between CSCs-EXOs and HT-29-EXOs treated groups. The p-values less than 0.05, 0.01, 0.001, and 0.0001 are shown using *, **, ***, and ****, respectively, on the graphs ( n = 3). C Comparative analysis of cell proliferation following 48 h treatment with CSC-derived exosomes (CSCs-EXOs), heat-inactivated exosomes (HI-EXOs; 95 °C for 10 min), or PBS as a control. Significant reductions in proliferation were observed in cells treated with CSC-EXOs, whereas HI-EXOs failed to induce this effect and showed proliferation levels comparable to the control (p-value < 0.01). These results indicate that the antiproliferative response depends on the biological activity and functional integrity of exosomal biomolecules. Data represent mean ± SD from three independent experiments; p < 0.05 versus the control
Exosome Treated Groups, supplied by Exosome Diagnostics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/exosome treated groups/product/Exosome Diagnostics
Average 86 stars, based on 1 article reviews
exosome treated groups - by Bioz Stars, 2026-06
86/100 stars
  Buy from Supplier

Image Search Results


Exosomal HMGB1 predicts poor prognosis in NSCLC. (A) A total of 80 NSCLC patients were categorised into metastasis ( n = 32) and nonmetastasis ( n = 48) groups. Blood‐derived exosomes were isolated, quantified and subjected to protein extraction for further analysis. A schematic workflow is presented. (B) Quantification of circulating exosome numbers in blood samples from the metastasis and nonmetastasis NSCLC patient groups. (C) Potential secretory protein factors within exosomes, particularly those implicated in lung cancer progression, were analysed. HMGB1 and Galectin‐9 was identified as a key candidate. A schematic diagram and quantification of exosomal TGF‐β, HMGB1, Galectin‐9 and MMP9 are shown. (D) Quantification of exosomal HMGB1 and galectin‐9 levels in the metastasis and nonmetastasis NSCLC groups. (E) Immunohistochemical (IHC) staining of HMGB1 in tumour tissues from patients with and without metastasis, followed by statistical analysis. (F) Correlation analysis between circulating exosomal HMGB1 concentrations and HMGB1 expression in tumour tissues from all 80 NSCLC patients. (G) Kaplan–Meier survival analysis based on HMGB1 expression in 558 NSCLC patients from the TCGA database. (H) Correlation analysis between HMGB1 expression and stemness scores across different cancer types using the Sanger database. (I) Heatmap showing expression of core stemness‐related genes (CD133, ALDH1, Nanog, Oct4, SOX2, KLF4, CD44) in tumour tissues from 12 NSCLC patients, stratified into HMGB1 low and HMGB1 high groups.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Exosomal HMGB1 predicts poor prognosis in NSCLC. (A) A total of 80 NSCLC patients were categorised into metastasis ( n = 32) and nonmetastasis ( n = 48) groups. Blood‐derived exosomes were isolated, quantified and subjected to protein extraction for further analysis. A schematic workflow is presented. (B) Quantification of circulating exosome numbers in blood samples from the metastasis and nonmetastasis NSCLC patient groups. (C) Potential secretory protein factors within exosomes, particularly those implicated in lung cancer progression, were analysed. HMGB1 and Galectin‐9 was identified as a key candidate. A schematic diagram and quantification of exosomal TGF‐β, HMGB1, Galectin‐9 and MMP9 are shown. (D) Quantification of exosomal HMGB1 and galectin‐9 levels in the metastasis and nonmetastasis NSCLC groups. (E) Immunohistochemical (IHC) staining of HMGB1 in tumour tissues from patients with and without metastasis, followed by statistical analysis. (F) Correlation analysis between circulating exosomal HMGB1 concentrations and HMGB1 expression in tumour tissues from all 80 NSCLC patients. (G) Kaplan–Meier survival analysis based on HMGB1 expression in 558 NSCLC patients from the TCGA database. (H) Correlation analysis between HMGB1 expression and stemness scores across different cancer types using the Sanger database. (I) Heatmap showing expression of core stemness‐related genes (CD133, ALDH1, Nanog, Oct4, SOX2, KLF4, CD44) in tumour tissues from 12 NSCLC patients, stratified into HMGB1 low and HMGB1 high groups.

Article Snippet: Mice treated with exosomal HMGB1 exhibited reduced sensitivity to PD‐1 blockade, and Annexin V/PI staining showed decreased tumour cell apoptosis in the exosome group (Figure ), suggesting that exosomal HMGB1 may contribute to immune evasion and resistance to immunotherapy.

Techniques: Derivative Assay, Isolation, Protein Extraction, Immunohistochemical staining, Immunohistochemistry, Expressing

Exosomal HMGB1 promotes NSCLC progression. (A) Western blot analysis of HMGB1 expression in vector control and HMGB1‐overexpressing (OE) A549 and PC9 cells. (B) Measurement of HMGB1 levels in exosomes derived from vector control and HMGB1 OE A549 and PC9 cells. (C) Cell proliferation assays of vector and HMGB1 OE A549 and PC9 cells. (D) Cell migration assays in vector and HMGB1 OE A549 and PC9 cells. (E) Colony formation assays for vector and HMGB1 OE A549 and PC9 cells. (F) Cell proliferation of A549 and PC9 cells treated with PBS, recombinant HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (G) Cell migration of A549 and PC9 cells under the same treatment conditions as in (F). (H) Colony formation capacity of A549 and PC9 cells under the same treatment conditions as in (F). (I) Tumour volume in A549‐bearing mice treated with PBS, HMGB1 (10 ng or 100 ng per mouse) or exosomes from vector or HMGB1 OE cells (1 × 10 10 exosomes per mouse). (J) A549 and PC9 cells were seeded at densities of 1 × 10 5 , 1 × 10 6 and 5 × 10 6 cells per six‐well plate and cultured for 3 days. Exosome production was then analysed.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Exosomal HMGB1 promotes NSCLC progression. (A) Western blot analysis of HMGB1 expression in vector control and HMGB1‐overexpressing (OE) A549 and PC9 cells. (B) Measurement of HMGB1 levels in exosomes derived from vector control and HMGB1 OE A549 and PC9 cells. (C) Cell proliferation assays of vector and HMGB1 OE A549 and PC9 cells. (D) Cell migration assays in vector and HMGB1 OE A549 and PC9 cells. (E) Colony formation assays for vector and HMGB1 OE A549 and PC9 cells. (F) Cell proliferation of A549 and PC9 cells treated with PBS, recombinant HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (G) Cell migration of A549 and PC9 cells under the same treatment conditions as in (F). (H) Colony formation capacity of A549 and PC9 cells under the same treatment conditions as in (F). (I) Tumour volume in A549‐bearing mice treated with PBS, HMGB1 (10 ng or 100 ng per mouse) or exosomes from vector or HMGB1 OE cells (1 × 10 10 exosomes per mouse). (J) A549 and PC9 cells were seeded at densities of 1 × 10 5 , 1 × 10 6 and 5 × 10 6 cells per six‐well plate and cultured for 3 days. Exosome production was then analysed.

Article Snippet: Mice treated with exosomal HMGB1 exhibited reduced sensitivity to PD‐1 blockade, and Annexin V/PI staining showed decreased tumour cell apoptosis in the exosome group (Figure ), suggesting that exosomal HMGB1 may contribute to immune evasion and resistance to immunotherapy.

Techniques: Western Blot, Expressing, Plasmid Preparation, Control, Derivative Assay, Migration, Recombinant, Cell Culture

Exosomal HMGB1 activates JAK/STAT3 signalling to promote NSCLC progression. (A) Protein–protein interaction (PPI) network analysis of HMGB1 using the STRING database. (B) Western blot analysis of NF‐κB in A549 and PC9 cells treated with PBS, recombinant HMGB1 (100 ng), exosomes from vector cells or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (C) ELISA quantification of IL‐6 in the supernatant of A549 and PC9 cells under the same treatment conditions as in (B). (D) Immunofluorescence staining of p‐STAT3 of A549 and PC9 cells under the same treatments, including an additional group co‐treated with exosomes from HMGB1 OE cells and NF‐κB inhibitor (50 μM). (E) Cell proliferation of A549 and PC9 cells treated with HMGB1 OE‐derived exosomes alone or in combination with NF‐κB inhibitor (50 μM) or STAT3 inhibitor (20 μM). (F) Cell migration under the same treatment conditions as in (E). (G) Colony formation assays of A549 and PC9 cells under the same treatment conditions as in (E).

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Exosomal HMGB1 activates JAK/STAT3 signalling to promote NSCLC progression. (A) Protein–protein interaction (PPI) network analysis of HMGB1 using the STRING database. (B) Western blot analysis of NF‐κB in A549 and PC9 cells treated with PBS, recombinant HMGB1 (100 ng), exosomes from vector cells or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (C) ELISA quantification of IL‐6 in the supernatant of A549 and PC9 cells under the same treatment conditions as in (B). (D) Immunofluorescence staining of p‐STAT3 of A549 and PC9 cells under the same treatments, including an additional group co‐treated with exosomes from HMGB1 OE cells and NF‐κB inhibitor (50 μM). (E) Cell proliferation of A549 and PC9 cells treated with HMGB1 OE‐derived exosomes alone or in combination with NF‐κB inhibitor (50 μM) or STAT3 inhibitor (20 μM). (F) Cell migration under the same treatment conditions as in (E). (G) Colony formation assays of A549 and PC9 cells under the same treatment conditions as in (E).

Article Snippet: Mice treated with exosomal HMGB1 exhibited reduced sensitivity to PD‐1 blockade, and Annexin V/PI staining showed decreased tumour cell apoptosis in the exosome group (Figure ), suggesting that exosomal HMGB1 may contribute to immune evasion and resistance to immunotherapy.

Techniques: Western Blot, Recombinant, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Derivative Assay, Migration

Targeting HMGB1 signalling improves therapeutic outcomes in NSCLC. (A) Correlation analysis between immune infiltration scores and HMGB1 expression in 491 LUAD and 500 LUSC patients from the TCGA database. (B) Correlation between HMGB1 expression and the distribution of various immune cell subsets in LUAD and LUSC patients. (C, D) THP‐1–derived M0 macrophages were treated with PBS, HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). M1 macrophage markers (CD86, CD80, iNOS) and M2 markers (CD206, IL‐10, Arg1) were quantified by PCR. (E) Lewis tumour‐bearing mice were treated with PBS, HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse, twice per week), anti‐PD‐1 antibody (RMP1‐14, 200 μg per mouse, twice per week) or combination therapy ( n = 5 per group). Tumour volumes and apoptosis levels in tumour tissues (day 25) were assessed. (F) PC9 cells were treated with PBS or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10), followed by Osimertinib (50 nM, 48 h), and apoptosis was measured. (G) A549 and PC9 cells were similarly treated with PBS or HMGB1 OE‐derived exosomes, followed by Cisplatin (5 μM, 48 h), and apoptosis was analysed. (H) A549 and PC9 cells were similarly treated with paclitaxel (10 μM, 48 h) under the same conditions, and cell apoptosis was determined. (I) A549‐bearing mice were treated with HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse), followed by PBS, paclitaxel (PTX, 10 mg/kg, twice per week), STAT3 inhibitor (5 mg/kg, twice per week) or combination therapy. (J) Schematic diagram illustrating the proposed mechanism: HMGB1 upregulates TLR4, thereby activating the NF‐κB–IL‐6 axis and stimulating JAK2/STAT3 signalling to promote tumour progression. Concurrently, HMGB1 facilitates M2 macrophage polarisation.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Targeting HMGB1 signalling improves therapeutic outcomes in NSCLC. (A) Correlation analysis between immune infiltration scores and HMGB1 expression in 491 LUAD and 500 LUSC patients from the TCGA database. (B) Correlation between HMGB1 expression and the distribution of various immune cell subsets in LUAD and LUSC patients. (C, D) THP‐1–derived M0 macrophages were treated with PBS, HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). M1 macrophage markers (CD86, CD80, iNOS) and M2 markers (CD206, IL‐10, Arg1) were quantified by PCR. (E) Lewis tumour‐bearing mice were treated with PBS, HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse, twice per week), anti‐PD‐1 antibody (RMP1‐14, 200 μg per mouse, twice per week) or combination therapy ( n = 5 per group). Tumour volumes and apoptosis levels in tumour tissues (day 25) were assessed. (F) PC9 cells were treated with PBS or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10), followed by Osimertinib (50 nM, 48 h), and apoptosis was measured. (G) A549 and PC9 cells were similarly treated with PBS or HMGB1 OE‐derived exosomes, followed by Cisplatin (5 μM, 48 h), and apoptosis was analysed. (H) A549 and PC9 cells were similarly treated with paclitaxel (10 μM, 48 h) under the same conditions, and cell apoptosis was determined. (I) A549‐bearing mice were treated with HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse), followed by PBS, paclitaxel (PTX, 10 mg/kg, twice per week), STAT3 inhibitor (5 mg/kg, twice per week) or combination therapy. (J) Schematic diagram illustrating the proposed mechanism: HMGB1 upregulates TLR4, thereby activating the NF‐κB–IL‐6 axis and stimulating JAK2/STAT3 signalling to promote tumour progression. Concurrently, HMGB1 facilitates M2 macrophage polarisation.

Article Snippet: Mice treated with exosomal HMGB1 exhibited reduced sensitivity to PD‐1 blockade, and Annexin V/PI staining showed decreased tumour cell apoptosis in the exosome group (Figure ), suggesting that exosomal HMGB1 may contribute to immune evasion and resistance to immunotherapy.

Techniques: Expressing, Derivative Assay, Plasmid Preparation

CSCs-, HT-29- and Caco-2-derived exosomes decreased the proliferation of Caco-2 and HT-29 cells. A Comparative analysis of Caco-2 cell proliferation after treatment with exosomes at different time intervals (24, 48, and 72 h) ( n = 3). As observed in the graph, exosome-treated groups (CSCs-, HT-29-, and Caco-2-derived exosomes) showed decreased cell proliferation compared to untreated groups and PBS. Cell proliferation was higher in cells treated with CSCs- derived exosomes compared to cells treated with HT-29-, and Caco-2-derived exosomes. B Comparative analysis of HT-29 cell proliferation after treatment with exosomes at 48 h ( n = 3). Exosome-treated groups showed a significant decrease in cell proliferation compared to untreated and PBS-treated groups. Following Bonferroni correction, the difference in cell proliferation was statistically significant ( p < 0.05) between CSCs-EXOs and HT-29-EXOs treated groups. The p-values less than 0.05, 0.01, 0.001, and 0.0001 are shown using *, **, ***, and ****, respectively, on the graphs ( n = 3). C Comparative analysis of cell proliferation following 48 h treatment with CSC-derived exosomes (CSCs-EXOs), heat-inactivated exosomes (HI-EXOs; 95 °C for 10 min), or PBS as a control. Significant reductions in proliferation were observed in cells treated with CSC-EXOs, whereas HI-EXOs failed to induce this effect and showed proliferation levels comparable to the control (p-value < 0.01). These results indicate that the antiproliferative response depends on the biological activity and functional integrity of exosomal biomolecules. Data represent mean ± SD from three independent experiments; p < 0.05 versus the control

Journal: Discover Oncology

Article Title: Functional role of cancer stem cell like exosomes on survival and drug resistance behaviors of colorectal cancer cells

doi: 10.1007/s12672-025-04295-0

Figure Lengend Snippet: CSCs-, HT-29- and Caco-2-derived exosomes decreased the proliferation of Caco-2 and HT-29 cells. A Comparative analysis of Caco-2 cell proliferation after treatment with exosomes at different time intervals (24, 48, and 72 h) ( n = 3). As observed in the graph, exosome-treated groups (CSCs-, HT-29-, and Caco-2-derived exosomes) showed decreased cell proliferation compared to untreated groups and PBS. Cell proliferation was higher in cells treated with CSCs- derived exosomes compared to cells treated with HT-29-, and Caco-2-derived exosomes. B Comparative analysis of HT-29 cell proliferation after treatment with exosomes at 48 h ( n = 3). Exosome-treated groups showed a significant decrease in cell proliferation compared to untreated and PBS-treated groups. Following Bonferroni correction, the difference in cell proliferation was statistically significant ( p < 0.05) between CSCs-EXOs and HT-29-EXOs treated groups. The p-values less than 0.05, 0.01, 0.001, and 0.0001 are shown using *, **, ***, and ****, respectively, on the graphs ( n = 3). C Comparative analysis of cell proliferation following 48 h treatment with CSC-derived exosomes (CSCs-EXOs), heat-inactivated exosomes (HI-EXOs; 95 °C for 10 min), or PBS as a control. Significant reductions in proliferation were observed in cells treated with CSC-EXOs, whereas HI-EXOs failed to induce this effect and showed proliferation levels comparable to the control (p-value < 0.01). These results indicate that the antiproliferative response depends on the biological activity and functional integrity of exosomal biomolecules. Data represent mean ± SD from three independent experiments; p < 0.05 versus the control

Article Snippet: B Comparative analysis showed that Caco-2 cell proliferation was significantly reduced after 5-FU treatment in exosome-treated groups (CSCs-, Caco-2- and HT-29-EXOs) compared to the control groups.

Techniques: Derivative Assay, Control, Activity Assay, Functional Assay

The cellular viability of Caco-2 cells treated with 5-FU chemotherapy drug and the effect of exosomes on drug cytotoxicity properties of Caco-2 cells. A IC50 and R2 square for different time points of 5-FU (24, 48, and 72 h) were 11.52 (R2 = 0.8148), 10.09 (R2 = 0.9020), and 6.4941 (R2 = 0.9130), respectively. Cellular viability was quantified by MTT assay. Data were recorded as the mean ± SD. B Comparative analysis showed that Caco-2 cell proliferation was significantly reduced after 5-FU treatment in exosome-treated groups (CSCs-, Caco-2- and HT-29-EXOs) compared to the control groups. While, cell proliferation was higher in cells treated with 5-FU + H29 CSCs-EXOs compared to cells treated with 5-FU + Caco-2-Exos and 5-FU + Caco-2-EXOs, but it was not statistically significant. P-values less than 0.05, 0.01, 0.001 and 0.0001 were shown using *, **, ***and ****, respectively, on the graphs ( n = 3)

Journal: Discover Oncology

Article Title: Functional role of cancer stem cell like exosomes on survival and drug resistance behaviors of colorectal cancer cells

doi: 10.1007/s12672-025-04295-0

Figure Lengend Snippet: The cellular viability of Caco-2 cells treated with 5-FU chemotherapy drug and the effect of exosomes on drug cytotoxicity properties of Caco-2 cells. A IC50 and R2 square for different time points of 5-FU (24, 48, and 72 h) were 11.52 (R2 = 0.8148), 10.09 (R2 = 0.9020), and 6.4941 (R2 = 0.9130), respectively. Cellular viability was quantified by MTT assay. Data were recorded as the mean ± SD. B Comparative analysis showed that Caco-2 cell proliferation was significantly reduced after 5-FU treatment in exosome-treated groups (CSCs-, Caco-2- and HT-29-EXOs) compared to the control groups. While, cell proliferation was higher in cells treated with 5-FU + H29 CSCs-EXOs compared to cells treated with 5-FU + Caco-2-Exos and 5-FU + Caco-2-EXOs, but it was not statistically significant. P-values less than 0.05, 0.01, 0.001 and 0.0001 were shown using *, **, ***and ****, respectively, on the graphs ( n = 3)

Article Snippet: B Comparative analysis showed that Caco-2 cell proliferation was significantly reduced after 5-FU treatment in exosome-treated groups (CSCs-, Caco-2- and HT-29-EXOs) compared to the control groups.

Techniques: MTT Assay, Control