Journal: Materials Today Bio

Article Title: Extracellular biogenic nanoscale mitochondria reprogram the wound microenvironment via ROS scavenging independent of cellular uptake

doi: 10.1016/j.mtbio.2026.103023

Figure Lengend Snippet: MSC-mt alleviates oxidative stress and promote tissue regeneration during wound healing (A) In vivo imaging showing the spatial–temporal persistence of fluorescently labeled MSC-mt (mtH) at the wound site at indicated time point, indicating transient but sustained early presence after topical application. (B) Measurement of ATP levels in peri-wound tissues on PWD8 showed enhanced local metabolic activity following mtH treatment. n = 5 ∼ 6 per group. (C) Quantification of malondialdehyde (MDA) levels in peri-wound tissues on PWD8 indicated reduced lipid peroxidation and oxidative stress in both MSC-mt–treated wounds. n = 5 ∼ 6 per group. (D) Laser speckle contrast imaging of blood perfusion at the wound site on PWD8 showed improved microvascular perfusion following mtH treatment. n = 5 per group. (E) Representative immunofluorescence images and quantification of CD31 expression in peri-wound tissues on PWD8, indicating enhanced angiogenesis in mtH–treated wounds. n = 6 per group. (F) Quantitative PCR analysis of angiogenesis-related gene expression in peri-wound tissues on PWD8, indicating transcriptional activation of pro-angiogenic programs following mtH treatment. n = 3 ∼ 5 per group. (G-H) Representative immunohistochemical staining and quantification of Col1a1 in wound tissues on PWD8, showing increased collagen synthesis and matrix remodeling in mtH–treated wounds. n = 6 per group. Scale bar = 100 μm. (I-J) Representative immunofluorescence staining and quantification of Vimentin and TUNEL in wound tissues on PWD8, indicating reduced fibroblast apoptosis following mtH treatment. n = 6 per group. Scale bar = 20 μm. (K-L) Representative immunofluorescence staining and quantification of Vimentin and 8-hydroxyguanosine (8-OHG) in wound tissues on PWD8, indicating attenuated oxidative DNA damage in fibroblasts following mtH treatment. n = 6 per group. Scale bar = 20 μm. Data are presented as mean ± SEM. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ns, not significant.

Article Snippet: For immunohistochemistry, Col1a1 expression was evaluated using a rabbit anti-Col1a1 antibody (CST, Cat# 72026, 1:200), followed by HRP-conjugated secondary antibody and DAB chromogen development.

Techniques: In Vivo Imaging, Labeling, Activity Assay, Imaging, Immunofluorescence, Expressing, Real-time Polymerase Chain Reaction, Gene Expression, Activation Assay, Immunohistochemical staining, Staining, TUNEL Assay

Journal: Frontiers in Oncology

Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

doi: 10.3389/fonc.2026.1784882

Figure Lengend Snippet: ADAMTS2 is coexpressed and physically interacts with COL1A1 in PCa. (A) Heatmap of the top 10 genes most strongly related to ADAMTS2 expression in the TCGA-PRAD cohort. (B) Scatter plot showing the correlation between ADAMTS2 and COL1A1 mRNA levels. (C) PPI network prediction from the STRING database indicating a potential interaction between ADAMTS2 and COL1A1. (D, E) Validation of COL1A1 mRNA ( n =6 pairs) and protein ( n =3 pairs) levels in paired human PCa and adjacent non-tumoral tissues using qRT-PCR and WB (paired two-tailed Student’s t-test). (F, G) Reciprocal Co-IP assessments illustrating physical interaction between endogenous and exogenously expressed ADAMTS2 and COL1A1 in DU145 cells. (H) WB of COL1A1 protein levels upon ADAMTS2 overexpression or knockdown in DU145 cells. (I) Evaluation of COL1A1 upregulation and downregulation effectiveness by WB in DU145 cells. Representative images from three independent experiments are shown. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3; unpaired two-tailed Student’s t-test). *P < 0.05, ***P < 0.001.

Article Snippet: The synthesis of primers for ADAMTS2, COL1A1, and other target genes was conducted by Sangon Biotech (China), and lists them.

Techniques: Expressing, Biomarker Discovery, Quantitative RT-PCR, Two Tailed Test, Co-Immunoprecipitation Assay, Over Expression, Knockdown

Journal: Frontiers in Oncology

Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

doi: 10.3389/fonc.2026.1784882

Figure Lengend Snippet: ADAMTS2 confers resistance to ferroptosis in PCa cells through COL1A1. (A) GSEA showing negative enrichment of ferroptosis-related gene signatures in TCGA-PRAD tumors with high ADAMTS2 expression. (B, C) Dose–response curves and IC 50 values for ferroptosis inducers erastin and RSL3 in control, ADAMTS2-overexpressing, and ADAMTS2-knockdown DU145 cells. IC 50 values were determined using non-linear regression analysis (n=3). (D) WB of SLC7A11 and GPX4 protein levels in ADAMTS2-knockdown cells in the presence or absence of COL1A1 overexpression. (E) WB of SLC7A11 and GPX4 in ADAMTS2-overexpressing cells in the presence or absence of COL1A1 knockdown. (F, G) MDA levels reflecting lipid peroxidation in the indicated cell groups. (H–K) Quantification of reduced GSH and oxidized GSSG under the specified genetic manipulations. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3). Statistical significance for multiple group comparisons was determined using one-way ANOVA followed by Tukey’s post hoc test. *P < 0.05.

Article Snippet: The synthesis of primers for ADAMTS2, COL1A1, and other target genes was conducted by Sangon Biotech (China), and lists them.

Techniques: Expressing, Control, Knockdown, Over Expression

Journal: Frontiers in Oncology

Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

doi: 10.3389/fonc.2026.1784882

Figure Lengend Snippet: Suppression of ADAMTS2 suppresses tumor growth in vivo and downregulates FAK/PI3K/AKT signaling and ferroptosis resistance markers. (A) Tumor growth curves of xenografts derived from control or ADAMTS2-knockdown DU145 cells in nude mice, evaluated every 7 days over 28 days. (n=5 mice per group). Statistical significance was determined using two-way ANOVA followed by Sidak’s multiple comparisons test. (B) Representative photographs and quantification of tumor weight at the experimental endpoint. Data are presented as the mean ± SD (n=5 mice per group; two-tailed Student’s t-test). (C) WB of ADAMTS2, p-FAK, FAK, p-PI3K, PI3K, COL1A1, p-AKT, AKT, SLC7A11, and GPX4 in excised xenograft tumor tissues. Representative blots from three independent tumor samples per group are shown. All quantitative data are presented as the mean ± SD. *P < 0.05.

Article Snippet: The synthesis of primers for ADAMTS2, COL1A1, and other target genes was conducted by Sangon Biotech (China), and lists them.

Techniques: In Vivo, Derivative Assay, Control, Knockdown, Two Tailed Test

Journal: Frontiers in Oncology

Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

doi: 10.3389/fonc.2026.1784882

Figure Lengend Snippet: ADAMTS2 is coexpressed and physically interacts with COL1A1 in PCa. (A) Heatmap of the top 10 genes most strongly related to ADAMTS2 expression in the TCGA-PRAD cohort. (B) Scatter plot showing the correlation between ADAMTS2 and COL1A1 mRNA levels. (C) PPI network prediction from the STRING database indicating a potential interaction between ADAMTS2 and COL1A1. (D, E) Validation of COL1A1 mRNA ( n =6 pairs) and protein ( n =3 pairs) levels in paired human PCa and adjacent non-tumoral tissues using qRT-PCR and WB (paired two-tailed Student’s t-test). (F, G) Reciprocal Co-IP assessments illustrating physical interaction between endogenous and exogenously expressed ADAMTS2 and COL1A1 in DU145 cells. (H) WB of COL1A1 protein levels upon ADAMTS2 overexpression or knockdown in DU145 cells. (I) Evaluation of COL1A1 upregulation and downregulation effectiveness by WB in DU145 cells. Representative images from three independent experiments are shown. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3; unpaired two-tailed Student’s t-test). *P < 0.05, ***P < 0.001.

Article Snippet: The lentiviral particles carrying ADAMTS2 or COL1A1 overexpression constructs, as well as short hairpin RNAs (shRNAs) targeting ADAMTS2 or COL1A1, were acquired from GeneChem (China).

Techniques: Expressing, Biomarker Discovery, Quantitative RT-PCR, Two Tailed Test, Co-Immunoprecipitation Assay, Over Expression, Knockdown

Journal: Frontiers in Oncology

Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

doi: 10.3389/fonc.2026.1784882

Figure Lengend Snippet: ADAMTS2 confers resistance to ferroptosis in PCa cells through COL1A1. (A) GSEA showing negative enrichment of ferroptosis-related gene signatures in TCGA-PRAD tumors with high ADAMTS2 expression. (B, C) Dose–response curves and IC 50 values for ferroptosis inducers erastin and RSL3 in control, ADAMTS2-overexpressing, and ADAMTS2-knockdown DU145 cells. IC 50 values were determined using non-linear regression analysis (n=3). (D) WB of SLC7A11 and GPX4 protein levels in ADAMTS2-knockdown cells in the presence or absence of COL1A1 overexpression. (E) WB of SLC7A11 and GPX4 in ADAMTS2-overexpressing cells in the presence or absence of COL1A1 knockdown. (F, G) MDA levels reflecting lipid peroxidation in the indicated cell groups. (H–K) Quantification of reduced GSH and oxidized GSSG under the specified genetic manipulations. All quantitative data are presented as the mean ± SD from three independent biological replicates (n=3). Statistical significance for multiple group comparisons was determined using one-way ANOVA followed by Tukey’s post hoc test. *P < 0.05.

Article Snippet: The lentiviral particles carrying ADAMTS2 or COL1A1 overexpression constructs, as well as short hairpin RNAs (shRNAs) targeting ADAMTS2 or COL1A1, were acquired from GeneChem (China).

Techniques: Expressing, Control, Knockdown, Over Expression

Journal: Frontiers in Oncology

Article Title: ADAMTS2 drives prostate cancer progression by activating FAK/PI3K/AKT signaling and suppressing ferroptosis via COL1A1

doi: 10.3389/fonc.2026.1784882

Figure Lengend Snippet: Suppression of ADAMTS2 suppresses tumor growth in vivo and downregulates FAK/PI3K/AKT signaling and ferroptosis resistance markers. (A) Tumor growth curves of xenografts derived from control or ADAMTS2-knockdown DU145 cells in nude mice, evaluated every 7 days over 28 days. (n=5 mice per group). Statistical significance was determined using two-way ANOVA followed by Sidak’s multiple comparisons test. (B) Representative photographs and quantification of tumor weight at the experimental endpoint. Data are presented as the mean ± SD (n=5 mice per group; two-tailed Student’s t-test). (C) WB of ADAMTS2, p-FAK, FAK, p-PI3K, PI3K, COL1A1, p-AKT, AKT, SLC7A11, and GPX4 in excised xenograft tumor tissues. Representative blots from three independent tumor samples per group are shown. All quantitative data are presented as the mean ± SD. *P < 0.05.

Article Snippet: The lentiviral particles carrying ADAMTS2 or COL1A1 overexpression constructs, as well as short hairpin RNAs (shRNAs) targeting ADAMTS2 or COL1A1, were acquired from GeneChem (China).

Techniques: In Vivo, Derivative Assay, Control, Knockdown, Two Tailed Test