Review

human b lymphoblastoid cell line tk6 (ATCC)

ATCC is a verified supplier

ATCC manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

ATCC human b lymphoblastoid cell line tk6
Micronucleus test of Kratom leaf extract after 4 h exposure with S9 in <t>TK6</t> cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Micronucleus test of Kratom leaf extract after 4 h exposure with S9 in <t>TK6</t> cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Human B Lymphoblastoid Cell Line Tk6, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 345 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human b lymphoblastoid cell line tk6/product/ATCC
Average 96 stars, based on 345 article reviews

human b lymphoblastoid cell line tk6 - by Bioz Stars, 2026-04

96/100 stars

Images

1) Product Images from "Genotoxicity risk assessment of a 7-hydroxymitragynine-enriched Kratom preparation: An integrated in silico and in vitro approach"

Article Title: Genotoxicity risk assessment of a 7-hydroxymitragynine-enriched Kratom preparation: An integrated in silico and in vitro approach

Journal: Toxicology Reports

doi: 10.1016/j.toxrep.2026.102206

Micronucleus test of Kratom leaf extract after 4 h exposure with S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Figure Legend Snippet: Micronucleus test of Kratom leaf extract after 4 h exposure with S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Techniques Used:

Micronucleus test of Kratom leaf extract after 4 h exposure without S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Figure Legend Snippet: Micronucleus test of Kratom leaf extract after 4 h exposure without S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Techniques Used:

Micronucleus test of Kratom leaf extract after 24 h exposure without S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Figure Legend Snippet: Micronucleus test of Kratom leaf extract after 24 h exposure without S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Techniques Used:

Image Search Results

Journal: Toxicology Reports

Article Title: Genotoxicity risk assessment of a 7-hydroxymitragynine-enriched Kratom preparation: An integrated in silico and in vitro approach

doi: 10.1016/j.toxrep.2026.102206

Figure Lengend Snippet: Micronucleus test of Kratom leaf extract after 4 h exposure with S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Article Snippet: The human B lymphoblastoid cell line (TK6) (CRL-8015; batch No. 70045146), purchased from ATCC, was cultured in RPMI 1640 medium supplemented with 10 % fetal bovine serum (FBS) and 1 % penicillin/streptomycin.

Techniques:

Journal: Toxicology Reports

Article Title: Genotoxicity risk assessment of a 7-hydroxymitragynine-enriched Kratom preparation: An integrated in silico and in vitro approach

doi: 10.1016/j.toxrep.2026.102206

Figure Lengend Snippet: Micronucleus test of Kratom leaf extract after 4 h exposure without S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Techniques:

Journal: Toxicology Reports

Article Title: Genotoxicity risk assessment of a 7-hydroxymitragynine-enriched Kratom preparation: An integrated in silico and in vitro approach

doi: 10.1016/j.toxrep.2026.102206

Figure Lengend Snippet: Micronucleus test of Kratom leaf extract after 24 h exposure without S9 in TK6 cells. Results are the mean ± SD of 3 independent experiments. Statistical testing with one-way ANOVA and Tukey’s post-hoc test (* p < 0.05).

Techniques:

Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of osteosarcoma. (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: Identification of active compounds and target prediction in YHD. (A) Venn diagram of the target of YHD and the target of osteosarcoma. (B – D) Gene Ontology (GO) enrichment analysis results. (E, F) Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis results. (G) The component-target-pathway-disease network implicated in the mechanism of YHD in osteosarcoma treatment. The triangles represent osteosarcoma, the diamonds represent pathways, the circles represent key genes, and the squares represent the active ingredients of YHD. (H) Heatmap of molecular docking score. A binding energy heatmap with a bluer color indicates a more stable binding. (I) Molecular docking visualization between the active components of YHD and key targets.

Article Snippet: Human osteosarcoma cell lines (HOS, 143B), human bone marrow stromal cells (HS-5), human proximal renal tubular epithelial cells (HK-2), and human normal liver cells (LO2) were all purchased from the American Type Culture Collection (ATCC).

Techniques: Binding Assay

YHD selectively inhibits osteosarcoma (OS) cells without affecting the viability or apoptosis of normal human cells. (A, B) CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (C, D) Colony formation assay detected the effect of YHD on the colony-forming ability of OS cells. (E – G) Flow cytometry was used to detect the effect of YHD on the cell cycle of OS cells. (H – J) Western blot analysis detected the effect of YHD on the levels of proliferation-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD selectively inhibits osteosarcoma (OS) cells without affecting the viability or apoptosis of normal human cells. (A, B) CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (C, D) Colony formation assay detected the effect of YHD on the colony-forming ability of OS cells. (E – G) Flow cytometry was used to detect the effect of YHD on the cell cycle of OS cells. (H – J) Western blot analysis detected the effect of YHD on the levels of proliferation-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Techniques: CCK-8 Assay, Colony Assay, Flow Cytometry, Western Blot, Standard Deviation

YHD can inhibit the migration and invasion of osteosarcoma (OS) cells, and promote their apoptosis. (A, B) Scratch healing assay showed that YHD inhibited the migration of OS cells. (C, D) Transwell assay showed that YHD inhibited the invasion of OS cells. (E – G) Western blot analysis detected the effect of YHD on the levels of proteins related to migration and invasion in OS cells. (H–K) Flow cytometry was used to detect the effect of YHD on apoptosis in OS cells. (L – N) Western blot analysis detected the effect of YHD on the levels of apoptosis-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD can inhibit the migration and invasion of osteosarcoma (OS) cells, and promote their apoptosis. (A, B) Scratch healing assay showed that YHD inhibited the migration of OS cells. (C, D) Transwell assay showed that YHD inhibited the invasion of OS cells. (E – G) Western blot analysis detected the effect of YHD on the levels of proteins related to migration and invasion in OS cells. (H–K) Flow cytometry was used to detect the effect of YHD on apoptosis in OS cells. (L – N) Western blot analysis detected the effect of YHD on the levels of apoptosis-related proteins in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Techniques: Migration, Transwell Assay, Western Blot, Flow Cytometry, Standard Deviation

YHD induces osteosarcoma (OS) cell death by increasing ROS levels. (A) The effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (B) After N-acetylcysteine (NAC) treatment, the effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (C) After NAC treatment, CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (D, E) After NAC treatment, scratch healing assay showed that YHD inhibited the migration of OS cells. (F, G) After NAC treatment, Transwell assay showed that YHD inhibited the invasion of OS cells. (H, I) After NAC treatment, flow cytometry was used to detect the effect of YHD on the apoptosis of OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD induces osteosarcoma (OS) cell death by increasing ROS levels. (A) The effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (B) After N-acetylcysteine (NAC) treatment, the effect of YHD on ROS levels in OS cells was detected using the DCFH probe method. (C) After NAC treatment, CCK8 assay detected the effect of YHD on the viability of OS cells at 24 h and 48 h. (D, E) After NAC treatment, scratch healing assay showed that YHD inhibited the migration of OS cells. (F, G) After NAC treatment, Transwell assay showed that YHD inhibited the invasion of OS cells. (H, I) After NAC treatment, flow cytometry was used to detect the effect of YHD on the apoptosis of OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Techniques: CCK-8 Assay, Migration, Transwell Assay, Flow Cytometry, Standard Deviation

YHD can induce mitochondrial dysfunction in osteosarcoma (OS) cells. (A) Real-time quantitative PCR was used to measure mitochondrial DNA (mtDNA) levels. (B, C) Western blot analysis detected the effect of YHD on the expression levels of proteins related to mitochondrial biogenesis in OS cells. (D, E) JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. (F, G) MitoSOX staining detected the effect of YHD on mitochondrial ROS levels in OS cells. (H) Seahorse XFe24 analyzer measured the effect of YHD on the oxygen consumption rate (OCR) in OS cells. (I) The effect of YHD on ATP content in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD can induce mitochondrial dysfunction in osteosarcoma (OS) cells. (A) Real-time quantitative PCR was used to measure mitochondrial DNA (mtDNA) levels. (B, C) Western blot analysis detected the effect of YHD on the expression levels of proteins related to mitochondrial biogenesis in OS cells. (D, E) JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. (F, G) MitoSOX staining detected the effect of YHD on mitochondrial ROS levels in OS cells. (H) Seahorse XFe24 analyzer measured the effect of YHD on the oxygen consumption rate (OCR) in OS cells. (I) The effect of YHD on ATP content in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Techniques: Real-time Polymerase Chain Reaction, Western Blot, Expressing, Staining, Membrane, Standard Deviation

YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Journal: Genes & Diseases

Article Title: Network pharmacology reveals that Yanghe Decoction inhibits osteosarcoma progression via ROS-induced mitochondrial dysfunction and enhances cisplatin sensitivity

doi: 10.1016/j.gendis.2025.101862

Figure Lengend Snippet: YHD exerts anti-tumor effects on osteosarcoma (OS) cells through the PI3K/AKT and p38 signaling pathways. (A) Principal component analysis revealed a clear distinction in gene expression profiles between the control and YHD groups. (B) Volcano plot identified 3495 differentially expressed genes in the YHD group. (C) Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. (D – G) Gene Set Enrichment Analysis (GSEA) of control and YHD groups. (H, I) Western blot analysis detected the effect of YHD on proteins related to the PI3K/AKT and MAPK pathways in OS cells. (J, K) After the addition of a PI3K activator and a P38 inhibitor, scratch healing assay showed that YHD inhibited the migration of OS cells. (L, M) After the addition of a PI3K activator and a P38 inhibitor, JC-1 staining detected the effect of YHD on the mitochondrial membrane potential in OS cells. Data were presented as mean ± standard deviation ( n = 3). ∗ p < 0.05 and ∗∗ p < 0.01 versus the blank group.

Techniques: Protein-Protein interactions, Gene Expression, Control, Western Blot, Migration, Staining, Membrane, Standard Deviation

EBA impairs cancer stem cell-like properties. (A) BT474 and SKBR3 cells were treated with EBA for 48 h, and ALDH1 activity was assessed by flow cytometry using the Aldefluor assay. DEAB was used to define the baseline of Aldefluor-positive fluorescence. (B) BT474 cells (5x10 4 cells/ml) were plated in ultra-low attachment dishes and cultured in the presence or absence of EBA for 5 days. The number and volume of mammospheres were measured by microscopy. (C) Overall survival of patients with breast cancer stratified by the co-expression of ALDH1A1 and CD44. (D) Spearman correlation analysis of ALDH1A1 and CD44 mRNA levels in patients with HER2-positive breast cancer from The Cancer Genome Atlas cohort (n=76). Kaplan-Meier survival analyses of patients with HER2-overexpressing breast cancer stratified by (E) ALDH1A1 and (F) CD44 expression. Patients were divided into high- and low-expression groups based on the median gene expression. Statistical significance was determined using the log-rank test. (G) JIMT-1 cells were treated with EBA (3 μ M) for 48 h and the CD44 high /CD24 low cell populations were identified by flow cytometry. (H) JIMT-1 cells (1.5x10 4 cells/ml) were cultured under serum-free suspension conditions in the presence of EBA (3 μ M) for 8 days. Mammosphere number and volumes were quantified. ** P<0.01 and **** P<0.0001 vs. vehicle-treated control (0 μ M EBA). EBA, ebastine; ALDH, aldehyde dehydrogenase; DEAB, diethylaminobenzaldehyde; CTL, control; ISO, isotype.

Journal: International Journal of Molecular Medicine

Article Title: Ebastine targets HER2/HER3 signaling and cancer stem cell traits to overcome trastuzumab resistance in HER2-positive breast cancer

doi: 10.3892/ijmm.2026.5751

Figure Lengend Snippet: EBA impairs cancer stem cell-like properties. (A) BT474 and SKBR3 cells were treated with EBA for 48 h, and ALDH1 activity was assessed by flow cytometry using the Aldefluor assay. DEAB was used to define the baseline of Aldefluor-positive fluorescence. (B) BT474 cells (5x10 4 cells/ml) were plated in ultra-low attachment dishes and cultured in the presence or absence of EBA for 5 days. The number and volume of mammospheres were measured by microscopy. (C) Overall survival of patients with breast cancer stratified by the co-expression of ALDH1A1 and CD44. (D) Spearman correlation analysis of ALDH1A1 and CD44 mRNA levels in patients with HER2-positive breast cancer from The Cancer Genome Atlas cohort (n=76). Kaplan-Meier survival analyses of patients with HER2-overexpressing breast cancer stratified by (E) ALDH1A1 and (F) CD44 expression. Patients were divided into high- and low-expression groups based on the median gene expression. Statistical significance was determined using the log-rank test. (G) JIMT-1 cells were treated with EBA (3 μ M) for 48 h and the CD44 high /CD24 low cell populations were identified by flow cytometry. (H) JIMT-1 cells (1.5x10 4 cells/ml) were cultured under serum-free suspension conditions in the presence of EBA (3 μ M) for 8 days. Mammosphere number and volumes were quantified. ** P<0.01 and **** P<0.0001 vs. vehicle-treated control (0 μ M EBA). EBA, ebastine; ALDH, aldehyde dehydrogenase; DEAB, diethylaminobenzaldehyde; CTL, control; ISO, isotype.

Article Snippet: The human breast cancer cell lines SKBR3, BT474, MDA-MB-453 (American Type Culture Collection) and JIMT-1 (Leibnitz Institute DSMZ-German Collection of Microorganisms and Cell Cultures GmbH) were cultured in DMEM, MEM or RPMI-1640 (all Sigma-Aldrich; Merck KGaA) supplemented with 10% FBS (Gibco; Thermo Fisher Scientific, Inc.) and 100 U/ml penicillin-streptomycin at 37°C in a humidified atmosphere of 5% CO 2 .

Techniques: Activity Assay, Flow Cytometry, Fluorescence, Cell Culture, Microscopy, Expressing, Gene Expression, Suspension, Control

VAX2 is upregulated and correlates with malignant progression in CRC. (A) Expression of VAX2 in the indicated CRC cell lines was determined by western blotting normalized to colon epithelial cell line FHC as a control. (B) Expression of VAX2 was determined in 13 pairs of CRC and normal tissues by western blotting using Wilcoxon signed-rank test. **, P < 0.05. (C) Expression of VAX2 was determined in 13 pairs of CRC and normal tissues by IHC. (D) Expression of VAX2 was determined in 79 pairs of CRC and normal tissues by IHC. (E) Quantitative expression of VAX2 in 79 pairs of CRC compared with normal tissues using Wilcoxon signed-rank test. ****, P < 0.001. (F) Quantitative expression of VAX2 in 99 CRC compared with 79 normal tissues using Mann–Whitney U test. ****, P < 0.001. (G) VAX2 expression levels in different subgroups stratified based on T stage. Mann–Whitney U test, **, P < 0.05. (H) VAX2 expression levels in different subgroups stratified based on AJCC stage. Mann–Whitney U test, **, P < 0.05. (I) Kaplan-Meier analyses of the overall survival probability in the TMA consisting of 99 patients based on VAX2 expression. Scale bars in C&D represent 100 μm.

Journal: Translational Oncology

Article Title: The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling

doi: 10.1016/j.tranon.2026.102703

Figure Lengend Snippet: VAX2 is upregulated and correlates with malignant progression in CRC. (A) Expression of VAX2 in the indicated CRC cell lines was determined by western blotting normalized to colon epithelial cell line FHC as a control. (B) Expression of VAX2 was determined in 13 pairs of CRC and normal tissues by western blotting using Wilcoxon signed-rank test. **, P < 0.05. (C) Expression of VAX2 was determined in 13 pairs of CRC and normal tissues by IHC. (D) Expression of VAX2 was determined in 79 pairs of CRC and normal tissues by IHC. (E) Quantitative expression of VAX2 in 79 pairs of CRC compared with normal tissues using Wilcoxon signed-rank test. ****, P < 0.001. (F) Quantitative expression of VAX2 in 99 CRC compared with 79 normal tissues using Mann–Whitney U test. ****, P < 0.001. (G) VAX2 expression levels in different subgroups stratified based on T stage. Mann–Whitney U test, **, P < 0.05. (H) VAX2 expression levels in different subgroups stratified based on AJCC stage. Mann–Whitney U test, **, P < 0.05. (I) Kaplan-Meier analyses of the overall survival probability in the TMA consisting of 99 patients based on VAX2 expression. Scale bars in C&D represent 100 μm.

Article Snippet: Normal colonic epithelial cell line FHC, human CRC cell lines (RKO, SW1116, HCT116 and SW620) and human GC cell lines (AGS) were purchased from the American Type Culture Collection (ATCC, USA; Catalog Numbers: FHC CRL-1831, RKO CRL-2577, SW1116 CCL-233, HCT116 CCL-247, SW620 CCL-227, AGS CRL-1739).

Techniques: Expressing, Western Blot, Control, MANN-WHITNEY

VAX2 facilitates CRC cell malignant behavior in vitro and in vivo. (A1/2) Expression of VAX2 in transfected LoVo, HCT116 and SW480 cell lines were analyzed by western blotting. (B1/2) Effects of VAX2 overexpression (B1) or knockdown (B2) on the proliferation of CRC cell lines, as determined by colony formation assay. ***, P < 0.01, Vector vs. VAX2; ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (C1/2) Representative graphs of EdU positivity in cells transfected with Vector and VAX2(C1) or Scr-siRNA and VAX2-siRNAp (C2). ***, P < 0.01, Vector vs. VAX2; ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (D1/2) Representative graphs of apoptosis assays in cells transfected with Vector and VAX2(D1) or Scr-siRNA and VAX2-siRNAp (D2). ****, P < 0.001, Vector vs. VAX2; ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (E1/2) Representative graphs of Transwell assays in cells transfected with Vector and VAX2(E1) or Scr-siRNA and VAX2-siRNAp (E2). ***, P < 0.01, Vector vs. VAX2; **, P < 0.05, ***, P < 0.01, Scr-siRNA vs. VAX2-siRNAp.

Journal: Translational Oncology

Article Title: The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling

doi: 10.1016/j.tranon.2026.102703

Figure Lengend Snippet: VAX2 facilitates CRC cell malignant behavior in vitro and in vivo. (A1/2) Expression of VAX2 in transfected LoVo, HCT116 and SW480 cell lines were analyzed by western blotting. (B1/2) Effects of VAX2 overexpression (B1) or knockdown (B2) on the proliferation of CRC cell lines, as determined by colony formation assay. ***, P < 0.01, Vector vs. VAX2; ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (C1/2) Representative graphs of EdU positivity in cells transfected with Vector and VAX2(C1) or Scr-siRNA and VAX2-siRNAp (C2). ***, P < 0.01, Vector vs. VAX2; ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (D1/2) Representative graphs of apoptosis assays in cells transfected with Vector and VAX2(D1) or Scr-siRNA and VAX2-siRNAp (D2). ****, P < 0.001, Vector vs. VAX2; ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (E1/2) Representative graphs of Transwell assays in cells transfected with Vector and VAX2(E1) or Scr-siRNA and VAX2-siRNAp (E2). ***, P < 0.01, Vector vs. VAX2; **, P < 0.05, ***, P < 0.01, Scr-siRNA vs. VAX2-siRNAp.

Techniques: In Vitro, In Vivo, Expressing, Transfection, Western Blot, Over Expression, Knockdown, Colony Assay, Plasmid Preparation

$VAX2 involves in WNT/beta-catenin signaling by promoting beta-catenin nucleus accumulation. (A&B) Kyoto Encyclopedia of Genes and Genomes (KEGG) (A) and Gene Set Enrichment Analysis (GSEA) (B) were conducted with differentially-expressed genes between Scr-siRNA and VAX2-siRNAp. (C) Western blotting of cytoplasmic and nuclear fractions of beta-catenin in VAX2 knockdown HCT116 cells. (D) Immunofluorescence of beta-catenin in VAX2 knockdown HCT116 and SW480 cells. (E) Co-immunoprecipitation of enrichment of beta-catenin binding to LEF1 in VAX2 knockdown HCT116 and SW480 cells. (F) qRT-PCR of abundance of beta-catenin-TCF/LEF-1 targets (MMP7, Cyclin D1 and c-jun) in VAX2 knockdown HCT116 and SW480 cells. **, P < 0.05, ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (G) VAX2-modulated CRC cells were transfected with the TOP/FOPflash reporter plasmid, and the reporter activities were determined 48 hours later ( n = 3). ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. Yellow scale bar in D, 50 μm; green scale bar in D, 20 μm.$

Journal: Translational Oncology

Article Title: The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling

doi: 10.1016/j.tranon.2026.102703

Figure Lengend Snippet: VAX2 involves in WNT/beta-catenin signaling by promoting beta-catenin nucleus accumulation. (A&B) Kyoto Encyclopedia of Genes and Genomes (KEGG) (A) and Gene Set Enrichment Analysis (GSEA) (B) were conducted with differentially-expressed genes between Scr-siRNA and VAX2-siRNAp. (C) Western blotting of cytoplasmic and nuclear fractions of beta-catenin in VAX2 knockdown HCT116 cells. (D) Immunofluorescence of beta-catenin in VAX2 knockdown HCT116 and SW480 cells. (E) Co-immunoprecipitation of enrichment of beta-catenin binding to LEF1 in VAX2 knockdown HCT116 and SW480 cells. (F) qRT-PCR of abundance of beta-catenin-TCF/LEF-1 targets (MMP7, Cyclin D1 and c-jun) in VAX2 knockdown HCT116 and SW480 cells. **, P < 0.05, ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (G) VAX2-modulated CRC cells were transfected with the TOP/FOPflash reporter plasmid, and the reporter activities were determined 48 hours later ( n = 3). ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. Yellow scale bar in D, 50 μm; green scale bar in D, 20 μm.

Techniques: Western Blot, Knockdown, Immunofluorescence, Immunoprecipitation, Binding Assay, Quantitative RT-PCR, Transfection, Plasmid Preparation

VAX2 transcriptionally activates SERPINE1 in gastrointestinal cancers. (A) Heatmap of top 10 upregulated and downregulated genes between Scr-siRNA and VAX2-siRNAp. (B) Volcano plot of differentially-expressed genes between Scr-siRNA and VAX2-siRNAp. (C) SERPINE1 abundance was detected between Scr-siRNA and VAX2-siRNAp in CRC cell lines via qRT-PCR. ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (D) SERPINE1 abundance was detected between Vector and VAX2 in LoVo via qRT-PCR. ***, P < 0.01, Vector vs. VAX2. (E1/2) SERPINE1 abundance was detected between Vector and VAX2 in AGS (E1) and HGC-27 (E2) cells via qRT-PCR. **, P < 0.05, ****, P < 0.001, Vector vs. VAX2. (F) Enrichment site and binding motif of VAX2 on SERPINE1 promotor predicted by Jaspar database. (G) Chromatin immunoprecipitation (ChIP) was performed in CRC cell lines HCT116 and SW480 and GC cell lines AGS. (H) Wildtype (WT) or mutation (MUT) SERPINE1 promotor was cloned into luciferase plasmids. (I) The WT or MUT SERPINE1 promoter construct was co-transfected with VAX2-siRNAp or Scr-siRNA in HCT116 and SW480 cells, and the relative luciferase activity to corresponding control was determined ( n = 3). *, P >0.05, ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (J) The WT or MUT SERPINE1 promoter construct was co-transfected with VAX2 or Vector in AGS cells, and the relative luciferase activity to corresponding control was determined ( n = 3). *, P >0.05, ***, P < 0.01, ****, P < 0.001, Vector vs. VAX2.

Journal: Translational Oncology

Article Title: The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling

doi: 10.1016/j.tranon.2026.102703

Figure Lengend Snippet: VAX2 transcriptionally activates SERPINE1 in gastrointestinal cancers. (A) Heatmap of top 10 upregulated and downregulated genes between Scr-siRNA and VAX2-siRNAp. (B) Volcano plot of differentially-expressed genes between Scr-siRNA and VAX2-siRNAp. (C) SERPINE1 abundance was detected between Scr-siRNA and VAX2-siRNAp in CRC cell lines via qRT-PCR. ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (D) SERPINE1 abundance was detected between Vector and VAX2 in LoVo via qRT-PCR. ***, P < 0.01, Vector vs. VAX2. (E1/2) SERPINE1 abundance was detected between Vector and VAX2 in AGS (E1) and HGC-27 (E2) cells via qRT-PCR. **, P < 0.05, ****, P < 0.001, Vector vs. VAX2. (F) Enrichment site and binding motif of VAX2 on SERPINE1 promotor predicted by Jaspar database. (G) Chromatin immunoprecipitation (ChIP) was performed in CRC cell lines HCT116 and SW480 and GC cell lines AGS. (H) Wildtype (WT) or mutation (MUT) SERPINE1 promotor was cloned into luciferase plasmids. (I) The WT or MUT SERPINE1 promoter construct was co-transfected with VAX2-siRNAp or Scr-siRNA in HCT116 and SW480 cells, and the relative luciferase activity to corresponding control was determined ( n = 3). *, P >0.05, ***, P < 0.01, ****, P < 0.001, Scr-siRNA vs. VAX2-siRNAp. (J) The WT or MUT SERPINE1 promoter construct was co-transfected with VAX2 or Vector in AGS cells, and the relative luciferase activity to corresponding control was determined ( n = 3). *, P >0.05, ***, P < 0.01, ****, P < 0.001, Vector vs. VAX2.

Techniques: Quantitative RT-PCR, Plasmid Preparation, Binding Assay, Chromatin Immunoprecipitation, Mutagenesis, Clone Assay, Luciferase, Construct, Transfection, Activity Assay, Control

VAX2 mediates CRC proliferation by transactivating SERPINE1 expression in vitro. (A) Proliferation of transfected CRC cell lines, as determined by colony formation assays. ****, P < 0.001. (B) Proliferation of transfected CRC cell lines, as determined by EdU assays. ****, P < 0.001. (C) Apoptosis of transfected CRC cell lines, as determined by apoptpsis assays using flow cytometry. (D) Co-immunoprecipitation of enrichment of beta-catenin binding to LEF1 in transfected HCT116 and SW480. (E) qRT-PCR of abundance of beta-catenin-TCF/LEF-1 targets (MMP7, Cyclin D1 and c-jun) in transfected HCT116 and SW480. **, P < 0.05, ***, P < 0.01, ****, P < 0.001.

Journal: Translational Oncology

Article Title: The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling

doi: 10.1016/j.tranon.2026.102703

Figure Lengend Snippet: VAX2 mediates CRC proliferation by transactivating SERPINE1 expression in vitro. (A) Proliferation of transfected CRC cell lines, as determined by colony formation assays. ****, P < 0.001. (B) Proliferation of transfected CRC cell lines, as determined by EdU assays. ****, P < 0.001. (C) Apoptosis of transfected CRC cell lines, as determined by apoptpsis assays using flow cytometry. (D) Co-immunoprecipitation of enrichment of beta-catenin binding to LEF1 in transfected HCT116 and SW480. (E) qRT-PCR of abundance of beta-catenin-TCF/LEF-1 targets (MMP7, Cyclin D1 and c-jun) in transfected HCT116 and SW480. **, P < 0.05, ***, P < 0.01, ****, P < 0.001.

Techniques: Expressing, In Vitro, Transfection, Flow Cytometry, Immunoprecipitation, Binding Assay, Quantitative RT-PCR

VAX2 is correlated with SERPINE1 in human CRC tissues. (A) Expression of VAX2 was determined in 71 pairs of CRC and NT by qRT-PCR using waterfall plot. (B) Expression of SERPINE1 was determined in 71 pairs of CRC and NT by qRT-PCR using waterfall plot. (C) Expression of VAX2 was determined in 71 pairs of CRC and NT by qRT-PCR using box plot. ****, P < 0.001. (D) Expression of SERPINE1 was determined in 71 pairs of CRC and NT by qRT-PCR using box plot. **, P < 0.05. (E) Correlation between VAX2 and SERPINE1 in 71 pairs CRC tissues. (F) Correlation between VAX2 and SERPINE1 in TCGA-CRC. (G) VAX2 and SERPINE1 expression in CRC tissues were detected using HE and IHC. ( H) The signal transduction mechanism of VAX2. Scale bar in G, 100 μm.

Journal: Translational Oncology

Article Title: The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling

doi: 10.1016/j.tranon.2026.102703

Figure Lengend Snippet: VAX2 is correlated with SERPINE1 in human CRC tissues. (A) Expression of VAX2 was determined in 71 pairs of CRC and NT by qRT-PCR using waterfall plot. (B) Expression of SERPINE1 was determined in 71 pairs of CRC and NT by qRT-PCR using waterfall plot. (C) Expression of VAX2 was determined in 71 pairs of CRC and NT by qRT-PCR using box plot. ****, P < 0.001. (D) Expression of SERPINE1 was determined in 71 pairs of CRC and NT by qRT-PCR using box plot. **, P < 0.05. (E) Correlation between VAX2 and SERPINE1 in 71 pairs CRC tissues. (F) Correlation between VAX2 and SERPINE1 in TCGA-CRC. (G) VAX2 and SERPINE1 expression in CRC tissues were detected using HE and IHC. ( H) The signal transduction mechanism of VAX2. Scale bar in G, 100 μm.

Techniques: Expressing, Quantitative RT-PCR, Transduction

HMGN1 inhibition affects the proliferation of cervical squamous cells. (A) mRNA and (B) protein expression levels of HMGN1 in SiHa and HeLa cells following siRNA transfection, compared with the NC. (C) Cell Counting Kit-8 assay assessing the proliferation of SiHa and HeLa cells at 24, 48 and 72 h. (D) Cell cycle distribution of SiHa and HeLa cells after HMGN1 inhibition was analyzed by flow cytometry, including flow cytometry plots and quantitative histograms. *P<0.05, **P<0.01 and ****P<0.001. HMGN1, high-mobility group nucleosome-binding protein 1; NC, non-targeting control; si, small interfering RNA.

Journal: Oncology Letters

Article Title: Lactylation-based machine algorithm combined with multi-omics analysis to predict prognosis in cervical cancer

doi: 10.3892/ol.2026.15486

Figure Lengend Snippet: HMGN1 inhibition affects the proliferation of cervical squamous cells. (A) mRNA and (B) protein expression levels of HMGN1 in SiHa and HeLa cells following siRNA transfection, compared with the NC. (C) Cell Counting Kit-8 assay assessing the proliferation of SiHa and HeLa cells at 24, 48 and 72 h. (D) Cell cycle distribution of SiHa and HeLa cells after HMGN1 inhibition was analyzed by flow cytometry, including flow cytometry plots and quantitative histograms. *P<0.05, **P<0.01 and ****P<0.001. HMGN1, high-mobility group nucleosome-binding protein 1; NC, non-targeting control; si, small interfering RNA.

Article Snippet: Human cervical squamous cell carcinoma cell lines SiHa (cat. no. HTB-35) and HeLa (cat. no. CRM-CCL-2) were obtained from the American Type Culture Collection and the human keratinocyte cell line HaCaT was obtained from The Cell Bank of Type Culture Collection of the Chinese Academy of Sciences (SCSP-5091; Beijing, China).

Techniques: Inhibition, Expressing, Transfection, Cell Counting, Flow Cytometry, Binding Assay, Control, Small Interfering RNA

MagGO induces tumor cell death via frequency- and mode-dependent mechanical disruption (A) TEM images of MagGO synthesized under MF. The dashed white line represents the contour edge of GO. Scale bars, 200 nm. (B) M-H curve of GO, MNP, and MagGO. (C) AFM image of MagGO and the height of GO in MagGO. Scale bars, 500 nm. (D, F, and H) Cell viability of U87 (D), MDA-MB-231 (F), and A549 (H) cells treated with MNP and MagGO under RMF and 3D MF (RMF combined with OMF stimulation) at 5 Hz. The applied field strength is 75 mT. The data were presented as the mean ± SD. (E, G, and I) Cell viability of U87 (E), MDA-MB-231 (G), and A549 (I) cells treated with MNP and MagGO under 3D MF of different frequencies. The applied field strength is 75 mT. The data were presented as the mean ± SD.

Journal: iScience

Article Title: An atom-edged magnetic nanomotor for cancer mechanotherapy

doi: 10.1016/j.isci.2026.114994

Figure Lengend Snippet: MagGO induces tumor cell death via frequency- and mode-dependent mechanical disruption (A) TEM images of MagGO synthesized under MF. The dashed white line represents the contour edge of GO. Scale bars, 200 nm. (B) M-H curve of GO, MNP, and MagGO. (C) AFM image of MagGO and the height of GO in MagGO. Scale bars, 500 nm. (D, F, and H) Cell viability of U87 (D), MDA-MB-231 (F), and A549 (H) cells treated with MNP and MagGO under RMF and 3D MF (RMF combined with OMF stimulation) at 5 Hz. The applied field strength is 75 mT. The data were presented as the mean ± SD. (E, G, and I) Cell viability of U87 (E), MDA-MB-231 (G), and A549 (I) cells treated with MNP and MagGO under 3D MF of different frequencies. The applied field strength is 75 mT. The data were presented as the mean ± SD.

Article Snippet: Glioblastoma U87 cells, human breast cancer cell line MDA-MB-231 cells, and human lung adenocarcinoma cell line A549 cells (American Type Culture Collection, Manassas, VA, USA) were cultured at 37°C under a humidified atmosphere containing 5% CO 2 with culture medium DMEM (Hyclone) containing of 1% penicillin and streptomycin (Hyclone) and 10% fetal bovine serum (FBS, Gibco).

Techniques: Disruption, Synthesized

MagGO induces lysosomal disruption (A) CLSM images of MNPs and MagGO in U87 cells. Lysosomes were stained with LysoTracker red (red), and the MNPs and MagGO were labeled with FITC (green). Scale bars, 15 μm. (B and C) Intensity profiles (white dashed line) of signals from lysosome and MNPs/MagGO fluorescent channels in (A). (D) CLSM images of MNPs and MagGO in MDA-MB-231 cells. Lysosomes were stained with LysoTracker red (red), and the MNPs and MagGO were labeled with FITC (green). Scale bars, 15 μm. (E and F) Intensity profiles (white dashed line) of signals from lysosomes and MNPs/MagGO fluorescent channels in (D). (G) CLSM images of MNPs and MagGO in A549 cells. Lysosomes were stained with LysoTracker red (red), and the MNPs and MagGO were labeled with FITC (green). Scale bars, 15 μm. (H and I) Intensity profiles (white dashed line) of signals from lysosomes and MNPs/MagGO fluorescent channels in (G). (J) CLSM images of U87 cells transfected with the EGFP-Gal3 plasmid after MagGO treatment under 3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 15 μm. (K) Counts of Gal3 puncta per U87 cell ( n = 10). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (L) Counts of Gal3 puncta per MDA-MB-231 cell ( n = 10). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (M) Counts of Gal3 puncta per A549 cell ( n = 10). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (N) Bio-TEM of lysosomal membrane morphology after mechanoporation for MagGO and MagGO+3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 1 μm. The dark blue arrow indicates the site of LMP, while the length of the blue arrow represents the size of the lysosomal membrane “wound”.

Journal: iScience

Article Title: An atom-edged magnetic nanomotor for cancer mechanotherapy

doi: 10.1016/j.isci.2026.114994

Figure Lengend Snippet: MagGO induces lysosomal disruption (A) CLSM images of MNPs and MagGO in U87 cells. Lysosomes were stained with LysoTracker red (red), and the MNPs and MagGO were labeled with FITC (green). Scale bars, 15 μm. (B and C) Intensity profiles (white dashed line) of signals from lysosome and MNPs/MagGO fluorescent channels in (A). (D) CLSM images of MNPs and MagGO in MDA-MB-231 cells. Lysosomes were stained with LysoTracker red (red), and the MNPs and MagGO were labeled with FITC (green). Scale bars, 15 μm. (E and F) Intensity profiles (white dashed line) of signals from lysosomes and MNPs/MagGO fluorescent channels in (D). (G) CLSM images of MNPs and MagGO in A549 cells. Lysosomes were stained with LysoTracker red (red), and the MNPs and MagGO were labeled with FITC (green). Scale bars, 15 μm. (H and I) Intensity profiles (white dashed line) of signals from lysosomes and MNPs/MagGO fluorescent channels in (G). (J) CLSM images of U87 cells transfected with the EGFP-Gal3 plasmid after MagGO treatment under 3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 15 μm. (K) Counts of Gal3 puncta per U87 cell ( n = 10). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (L) Counts of Gal3 puncta per MDA-MB-231 cell ( n = 10). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (M) Counts of Gal3 puncta per A549 cell ( n = 10). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (N) Bio-TEM of lysosomal membrane morphology after mechanoporation for MagGO and MagGO+3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 1 μm. The dark blue arrow indicates the site of LMP, while the length of the blue arrow represents the size of the lysosomal membrane “wound”.

Techniques: Disruption, Staining, Labeling, Transfection, Plasmid Preparation, Membrane

MagGO primarily induces pyroptosis as the mode of cell death (A–C) CLSM images of CTSB release of U87 (A), MDA-MB-231 (B), and A549 (C) cells after MagGO treatment under 3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 20 μm. (D–F) The cell viabilities of U87 (D), MDA-MB-231 (E), and A549 (F) cells treated with MagGO were assessed after pre-treatment with z-VAD-FMK (10 μM), Necrostatin-1 (10 μM), 3-Methyladenine (10 μM), Ferrostatin-1 (2 μM), and MCC950 (10 nM) for 4 h, followed by exposure to 3D MF at 5 Hz for 30 min. The applied field strength was 75 mT. The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (G and H) Quantification of IL-1β (G) and IL-18 (H) release from U87 cells for control, MagGO, and MagGO+3D MF ( n = 3). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (I and J) Western blot analysis of Casp-1 (I) and GSDMD (J) in U87 cells for control, MagGO, and MagGO+3D MF.

Journal: iScience

Article Title: An atom-edged magnetic nanomotor for cancer mechanotherapy

doi: 10.1016/j.isci.2026.114994

Figure Lengend Snippet: MagGO primarily induces pyroptosis as the mode of cell death (A–C) CLSM images of CTSB release of U87 (A), MDA-MB-231 (B), and A549 (C) cells after MagGO treatment under 3D MF. The applied field strength is 75 mT. The duration of magnetic field application is 30 min. Scale bars, 20 μm. (D–F) The cell viabilities of U87 (D), MDA-MB-231 (E), and A549 (F) cells treated with MagGO were assessed after pre-treatment with z-VAD-FMK (10 μM), Necrostatin-1 (10 μM), 3-Methyladenine (10 μM), Ferrostatin-1 (2 μM), and MCC950 (10 nM) for 4 h, followed by exposure to 3D MF at 5 Hz for 30 min. The applied field strength was 75 mT. The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (G and H) Quantification of IL-1β (G) and IL-18 (H) release from U87 cells for control, MagGO, and MagGO+3D MF ( n = 3). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post-hoc test. (I and J) Western blot analysis of Casp-1 (I) and GSDMD (J) in U87 cells for control, MagGO, and MagGO+3D MF.

Techniques: Control, Western Blot

Broad antitumor activity of MagGO across multiple tumor models (A) Schematic illustrations of in vivo anticancer therapy for MDA-MB-231 and A549 tumors. The applied field strength is 75 mT. The applied field frequency is 5 Hz. The duration of magnetic field application is 30 min. (B) The MDA-MB-231 tumor volume comparison of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF for 14 days ( n = 5). (C) The MDA-MB-231 tumor images of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). (D) The MDA-MB-231 tumor weight of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (E) The MDA-MB-231 tumor volume of each mouse in the control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF groups for 14 days. (F) The A549 tumor volume comparison of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF for 14 days ( n = 5). (G) The A549 tumor images of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). (H) The A549 tumor weight of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (I) The A549 tumor volume of each mouse in the control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF groups for 14 days.

Journal: iScience

Article Title: An atom-edged magnetic nanomotor for cancer mechanotherapy

doi: 10.1016/j.isci.2026.114994

Figure Lengend Snippet: Broad antitumor activity of MagGO across multiple tumor models (A) Schematic illustrations of in vivo anticancer therapy for MDA-MB-231 and A549 tumors. The applied field strength is 75 mT. The applied field frequency is 5 Hz. The duration of magnetic field application is 30 min. (B) The MDA-MB-231 tumor volume comparison of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF for 14 days ( n = 5). (C) The MDA-MB-231 tumor images of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). (D) The MDA-MB-231 tumor weight of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (E) The MDA-MB-231 tumor volume of each mouse in the control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF groups for 14 days. (F) The A549 tumor volume comparison of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF for 14 days ( n = 5). (G) The A549 tumor images of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). (H) The A549 tumor weight of control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF ( n = 5). The data were presented as the mean ± SD. Data were analyzed by one-way ANOVA with Tukey’s post hoc test. (I) The A549 tumor volume of each mouse in the control, MNP, MagGO, MNP+3D MF, and MagGO+3D MF groups for 14 days.

Techniques: Activity Assay, In Vivo, Comparison, Control

Review

Structured Review

Images

1) Product Images from "Genotoxicity risk assessment of a 7-hydroxymitragynine-enriched Kratom preparation: An integrated in silico and in vitro approach"

Similar Products

Image Search Results