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The exploration for the role of SNHG7 in cuproptosis. A. qPCR validation of the differential expression levels of SNHG7 between normal and CRC patient tumor tissue (n=3, paired t-test). B. qPCR validation of the differential expression levels of SNHG7 between CRC cell lines and normal cells (n=3, paired t-test). C-D. CRC cell cell lines were transfected with siRN or overexpression plasmids to construct SNHG7 knockdown or overexpression cell lines. E. qPCR validation of SNHG7 expression levels in the occurrence of cuproptosis (n=3, paired t-test). F-G. Lactate production assay was used for detecting the level of the glycolysis in CRC cells with SNHG7-siRNA and overexpression compared with the control group (n=3, paired t-test). H. Viability of CRC cells in SNHG7 overexpression and PCBP2 knockdown on cuproptosis under varying concentrations of ESCu (n=3, one-way ANOVA). I-L. Viability of CRC cells in control and SNHG7-siRNA and overexpression groups after treatment with ESCu. M-O. Identifying associations among SNHG7, PCBP2, and <t>CDKN2A</t> using the GEPIA database (n=3, one-way ANOVA). P-R. Expression changes of SNHG7, PCBP2, and CDKN2A upon SNHG7 overexpression or CDKN2A knockdown by qPCR (n=3, paired t-test). S-T. Western blot analysis confirmed changes in PCBP2 and <t>CDKN2A</t> <t>protein</t> expression following SNHG7 overexpression or PCBP2 silencing in colorectal cancer cell lines. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
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The exploration for the role of SNHG7 in cuproptosis. A. qPCR validation of the differential expression levels of SNHG7 between normal and CRC patient tumor tissue (n=3, paired t-test). B. qPCR validation of the differential expression levels of SNHG7 between CRC cell lines and normal cells (n=3, paired t-test). C-D. CRC cell cell lines were transfected with siRN or overexpression plasmids to construct SNHG7 knockdown or overexpression cell lines. E. qPCR validation of SNHG7 expression levels in the occurrence of cuproptosis (n=3, paired t-test). F-G. Lactate production assay was used for detecting the level of the glycolysis in CRC cells with SNHG7-siRNA and overexpression compared with the control group (n=3, paired t-test). H. Viability of CRC cells in SNHG7 overexpression and PCBP2 knockdown on cuproptosis under varying concentrations of ESCu (n=3, one-way ANOVA). I-L. Viability of CRC cells in control and SNHG7-siRNA and overexpression groups after treatment with ESCu. M-O. Identifying associations among SNHG7, PCBP2, and <t>CDKN2A</t> using the GEPIA database (n=3, one-way ANOVA). P-R. Expression changes of SNHG7, PCBP2, and CDKN2A upon SNHG7 overexpression or CDKN2A knockdown by qPCR (n=3, paired t-test). S-T. Western blot analysis confirmed changes in PCBP2 and <t>CDKN2A</t> <t>protein</t> expression following SNHG7 overexpression or PCBP2 silencing in colorectal cancer cell lines. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).
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Caudal discs of SM/J mice evidence early cellular senescence and a senescence signature during degeneration. At four weeks of age, SM/J mice have increase abundance of senescence markers in their caudal discs, evidenced by ( a–a” ) p19 and ( b–b” ) <t>p21</t> abundance relative to age-matched B6J discs. c Microarray analysis of 4-week-old and 17-week-old SM/J NP and AF shows distinct clustering in both tissues between the two timepoints. Thematic analysis in CompBio of enriched concepts in 17-week-old NP tissues, compared to 4-week-old tissues shows: ( d’ ) Beta-galactoside Alpha-2,3-sialytransferase Activity is an upregulated theme in the NP; ( e ) VEGF-A Complex is an upregulated theme in the AF; ( f ) CDK1 Phosphorylates Condensin is a downregulated theme in the NP; and ( g ) RUNX2 Regulates Osteoblast Differentiation is a downregulated theme in the AF. h Venn Diagram showing the gene-level overlap between SM/J tissue profiles and the SenMayo geneset, with the overlapping genes shown in ( i ). Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. n C57BL/6J 4w = 8; n SM/J 4w = 5; n SM/J 17w = 6
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The exploration for the role of SNHG7 in cuproptosis. A. qPCR validation of the differential expression levels of SNHG7 between normal and CRC patient tumor tissue (n=3, paired t-test). B. qPCR validation of the differential expression levels of SNHG7 between CRC cell lines and normal cells (n=3, paired t-test). C-D. CRC cell cell lines were transfected with siRN or overexpression plasmids to construct SNHG7 knockdown or overexpression cell lines. E. qPCR validation of SNHG7 expression levels in the occurrence of cuproptosis (n=3, paired t-test). F-G. Lactate production assay was used for detecting the level of the glycolysis in CRC cells with SNHG7-siRNA and overexpression compared with the control group (n=3, paired t-test). H. Viability of CRC cells in SNHG7 overexpression and PCBP2 knockdown on cuproptosis under varying concentrations of ESCu (n=3, one-way ANOVA). I-L. Viability of CRC cells in control and SNHG7-siRNA and overexpression groups after treatment with ESCu. M-O. Identifying associations among SNHG7, PCBP2, and CDKN2A using the GEPIA database (n=3, one-way ANOVA). P-R. Expression changes of SNHG7, PCBP2, and CDKN2A upon SNHG7 overexpression or CDKN2A knockdown by qPCR (n=3, paired t-test). S-T. Western blot analysis confirmed changes in PCBP2 and CDKN2A protein expression following SNHG7 overexpression or PCBP2 silencing in colorectal cancer cell lines. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Translational Oncology

Article Title: SNHG7 interacts with PCBP2 to promote CDKN2A expression and modulate cuproptosis in colorectal cancer

doi: 10.1016/j.tranon.2026.102724

Figure Lengend Snippet: The exploration for the role of SNHG7 in cuproptosis. A. qPCR validation of the differential expression levels of SNHG7 between normal and CRC patient tumor tissue (n=3, paired t-test). B. qPCR validation of the differential expression levels of SNHG7 between CRC cell lines and normal cells (n=3, paired t-test). C-D. CRC cell cell lines were transfected with siRN or overexpression plasmids to construct SNHG7 knockdown or overexpression cell lines. E. qPCR validation of SNHG7 expression levels in the occurrence of cuproptosis (n=3, paired t-test). F-G. Lactate production assay was used for detecting the level of the glycolysis in CRC cells with SNHG7-siRNA and overexpression compared with the control group (n=3, paired t-test). H. Viability of CRC cells in SNHG7 overexpression and PCBP2 knockdown on cuproptosis under varying concentrations of ESCu (n=3, one-way ANOVA). I-L. Viability of CRC cells in control and SNHG7-siRNA and overexpression groups after treatment with ESCu. M-O. Identifying associations among SNHG7, PCBP2, and CDKN2A using the GEPIA database (n=3, one-way ANOVA). P-R. Expression changes of SNHG7, PCBP2, and CDKN2A upon SNHG7 overexpression or CDKN2A knockdown by qPCR (n=3, paired t-test). S-T. Western blot analysis confirmed changes in PCBP2 and CDKN2A protein expression following SNHG7 overexpression or PCBP2 silencing in colorectal cancer cell lines. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: The primary antibodies used included PCBP2 (15070-1-AP, Proteintech; 1:1000) and CDKN2A (AF5484, Affinity; 1:1000), with incubation at 4°C overnight.

Techniques: Biomarker Discovery, Quantitative Proteomics, Transfection, Over Expression, Construct, Knockdown, Expressing, Control, Western Blot

Association between SNHG7, PCBP2 and CDKN2A. A-D. RNA from SW480 cells was immunoprecipitated using an anti-PCBP2 antibody, followed by qPCR and agarose gel assays to confirm the binding of PCBP2 to SNHG7 and CDKN2A (n=3, paired t-test). E-H. Western blot analysis confirmed changes in PCBP2 and CDKN2A protein expression following SNHG7 silencing or overexpression in colorectal cancer cell lines. I-L. Similarly, qPCR assays validated alterations in PCBP2 and CDKN2A RNA levels under the same conditions (n=3, paired t-test). M-N. qPCR validation of PCBP2 and CDKN2A expression levels in the occurrence of cuproptosis (n=3, paired t-test). O-P. Changes in the expression levels of distinct exons of SNHG7 and CDKN2A upon overexpression (n=3, paired t-test). (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Translational Oncology

Article Title: SNHG7 interacts with PCBP2 to promote CDKN2A expression and modulate cuproptosis in colorectal cancer

doi: 10.1016/j.tranon.2026.102724

Figure Lengend Snippet: Association between SNHG7, PCBP2 and CDKN2A. A-D. RNA from SW480 cells was immunoprecipitated using an anti-PCBP2 antibody, followed by qPCR and agarose gel assays to confirm the binding of PCBP2 to SNHG7 and CDKN2A (n=3, paired t-test). E-H. Western blot analysis confirmed changes in PCBP2 and CDKN2A protein expression following SNHG7 silencing or overexpression in colorectal cancer cell lines. I-L. Similarly, qPCR assays validated alterations in PCBP2 and CDKN2A RNA levels under the same conditions (n=3, paired t-test). M-N. qPCR validation of PCBP2 and CDKN2A expression levels in the occurrence of cuproptosis (n=3, paired t-test). O-P. Changes in the expression levels of distinct exons of SNHG7 and CDKN2A upon overexpression (n=3, paired t-test). (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: The primary antibodies used included PCBP2 (15070-1-AP, Proteintech; 1:1000) and CDKN2A (AF5484, Affinity; 1:1000), with incubation at 4°C overnight.

Techniques: Immunoprecipitation, Agarose Gel Electrophoresis, Binding Assay, Western Blot, Expressing, Over Expression, Biomarker Discovery

In vivo validation of the relationship among SNHG7, PCBP2, and CDKN2A. SNHG7 promotes tumor growth. BALB/c nude mice were subcutaneously injected with 5 × 10⁶ normal or SNHG7-overexpressing cells, with half of the mice in each group receiving intraperitoneal injections of ESCu (1 mg/kg). Tumor size was measured every days. A-C. Alterations in subcutaneous tumor volume in BALB/c nude mice (n=5, two-way ANOVA). D. Western blot analysis was performed to evaluate PCBP2 and CDKN2A protein expression in subcutaneous tumors from each group of nude mice. E-G. qPCR analysis was conducted to assess RNA level changes of SNHG7, PCBP2 and CDKN2A in subcutaneous tumors (n=5, paired t-test). H-M. Protein expression of PCBP2, CDKN2A, and Ki67 was evaluated by IHC staining (scale bars: 50 μm, 20 μm). Data are presented as mean ± SD (* p < 0.05, ** p < 0.01). Each group included five biological replicates in animal experiments. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Journal: Translational Oncology

Article Title: SNHG7 interacts with PCBP2 to promote CDKN2A expression and modulate cuproptosis in colorectal cancer

doi: 10.1016/j.tranon.2026.102724

Figure Lengend Snippet: In vivo validation of the relationship among SNHG7, PCBP2, and CDKN2A. SNHG7 promotes tumor growth. BALB/c nude mice were subcutaneously injected with 5 × 10⁶ normal or SNHG7-overexpressing cells, with half of the mice in each group receiving intraperitoneal injections of ESCu (1 mg/kg). Tumor size was measured every days. A-C. Alterations in subcutaneous tumor volume in BALB/c nude mice (n=5, two-way ANOVA). D. Western blot analysis was performed to evaluate PCBP2 and CDKN2A protein expression in subcutaneous tumors from each group of nude mice. E-G. qPCR analysis was conducted to assess RNA level changes of SNHG7, PCBP2 and CDKN2A in subcutaneous tumors (n=5, paired t-test). H-M. Protein expression of PCBP2, CDKN2A, and Ki67 was evaluated by IHC staining (scale bars: 50 μm, 20 μm). Data are presented as mean ± SD (* p < 0.05, ** p < 0.01). Each group included five biological replicates in animal experiments. (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001).

Article Snippet: The primary antibodies used included PCBP2 (15070-1-AP, Proteintech; 1:1000) and CDKN2A (AF5484, Affinity; 1:1000), with incubation at 4°C overnight.

Techniques: In Vivo, Biomarker Discovery, Injection, Western Blot, Expressing, Immunohistochemistry

Schematic diagram of the molecular mechanism of this study Elevated levels of SNHG7 serve as a prognostic marker in colorectal cancer patients. Mechanistically, SNHG7 directly binds to the RNA-binding protein PCBP2 and promotes the expression of CDKN2A which inhibits cuproptosis. Additionally, increased SNHG7 levels enhance lactate expression and further suppress cuproptosis.

Journal: Translational Oncology

Article Title: SNHG7 interacts with PCBP2 to promote CDKN2A expression and modulate cuproptosis in colorectal cancer

doi: 10.1016/j.tranon.2026.102724

Figure Lengend Snippet: Schematic diagram of the molecular mechanism of this study Elevated levels of SNHG7 serve as a prognostic marker in colorectal cancer patients. Mechanistically, SNHG7 directly binds to the RNA-binding protein PCBP2 and promotes the expression of CDKN2A which inhibits cuproptosis. Additionally, increased SNHG7 levels enhance lactate expression and further suppress cuproptosis.

Article Snippet: The primary antibodies used included PCBP2 (15070-1-AP, Proteintech; 1:1000) and CDKN2A (AF5484, Affinity; 1:1000), with incubation at 4°C overnight.

Techniques: Marker, RNA Binding Assay, Expressing

Caudal discs of SM/J mice evidence early cellular senescence and a senescence signature during degeneration. At four weeks of age, SM/J mice have increase abundance of senescence markers in their caudal discs, evidenced by ( a–a” ) p19 and ( b–b” ) p21 abundance relative to age-matched B6J discs. c Microarray analysis of 4-week-old and 17-week-old SM/J NP and AF shows distinct clustering in both tissues between the two timepoints. Thematic analysis in CompBio of enriched concepts in 17-week-old NP tissues, compared to 4-week-old tissues shows: ( d’ ) Beta-galactoside Alpha-2,3-sialytransferase Activity is an upregulated theme in the NP; ( e ) VEGF-A Complex is an upregulated theme in the AF; ( f ) CDK1 Phosphorylates Condensin is a downregulated theme in the NP; and ( g ) RUNX2 Regulates Osteoblast Differentiation is a downregulated theme in the AF. h Venn Diagram showing the gene-level overlap between SM/J tissue profiles and the SenMayo geneset, with the overlapping genes shown in ( i ). Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. n C57BL/6J 4w = 8; n SM/J 4w = 5; n SM/J 17w = 6

Journal: Bone Research

Article Title: Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice

doi: 10.1038/s41413-026-00526-4

Figure Lengend Snippet: Caudal discs of SM/J mice evidence early cellular senescence and a senescence signature during degeneration. At four weeks of age, SM/J mice have increase abundance of senescence markers in their caudal discs, evidenced by ( a–a” ) p19 and ( b–b” ) p21 abundance relative to age-matched B6J discs. c Microarray analysis of 4-week-old and 17-week-old SM/J NP and AF shows distinct clustering in both tissues between the two timepoints. Thematic analysis in CompBio of enriched concepts in 17-week-old NP tissues, compared to 4-week-old tissues shows: ( d’ ) Beta-galactoside Alpha-2,3-sialytransferase Activity is an upregulated theme in the NP; ( e ) VEGF-A Complex is an upregulated theme in the AF; ( f ) CDK1 Phosphorylates Condensin is a downregulated theme in the NP; and ( g ) RUNX2 Regulates Osteoblast Differentiation is a downregulated theme in the AF. h Venn Diagram showing the gene-level overlap between SM/J tissue profiles and the SenMayo geneset, with the overlapping genes shown in ( i ). Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. n C57BL/6J 4w = 8; n SM/J 4w = 5; n SM/J 17w = 6

Article Snippet: Tissue sections were then blocked in 2%–10% normal serum in PBS-T, and incubated with antibodies against p19 (1:100, Novus NB200-106), p21 (1:200, Novus NB100-1941), collagen I (1:100, Abcam ab34710), aggrecan (1:50; Millipore; AB1031), chondroitin sulfate (1:300, Abcam ab11570), IL-1b (1:100, Novus NB600-633), IL-6 (1:50, Novus NB600-1131), TGFb (1:100; Abcam; ab92486), collagen X (1:500, Abcam ab58632), CA3 (1:150, Santa Cruz), and GLUT-1 (1:200, Abcam, ab40084).

Techniques: Microarray, Activity Assay, MANN-WHITNEY

DQ reduces caudal disc degeneration and senescence in SM/J mice. a , b Schematic showing study design: intraperitoneal injections of DQ, Nav., or a Vehicle control were administered once every week to mice starting at 4 weeks of age and ending at 17 weeks of age. a’ –a’” SafraninO/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows DQ improves disc degeneration in SM/J mice. Images reflect the range of degenerative outcomes across treatment cohorts. b’ –b” Safranin/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows Nav. does not improve disc degeneration in SM/J mice. Quantitative immunohistochemistry shows reduced ( c–c” ) p19 (NP and AF) and ( d–d” ) p21 (AF only) in DQ-treated SM/J discs. SASP markers of ( e–e” ) TGF β, ( f–f” ) IL-6, ( g–g” ) MMP13, and ( h–h” ) IL-1β indicate DQ mediates SASP in SM/J discs. Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. Distribution statistics were determined using a χ 2 test. 17 weeks old ( n DQ = 11, 6 females + 5 males; n CT = 13, 6 females + 7 males; n Nav. = 7, n Veh. = 7)

Journal: Bone Research

Article Title: Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice

doi: 10.1038/s41413-026-00526-4

Figure Lengend Snippet: DQ reduces caudal disc degeneration and senescence in SM/J mice. a , b Schematic showing study design: intraperitoneal injections of DQ, Nav., or a Vehicle control were administered once every week to mice starting at 4 weeks of age and ending at 17 weeks of age. a’ –a’” SafraninO/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows DQ improves disc degeneration in SM/J mice. Images reflect the range of degenerative outcomes across treatment cohorts. b’ –b” Safranin/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows Nav. does not improve disc degeneration in SM/J mice. Quantitative immunohistochemistry shows reduced ( c–c” ) p19 (NP and AF) and ( d–d” ) p21 (AF only) in DQ-treated SM/J discs. SASP markers of ( e–e” ) TGF β, ( f–f” ) IL-6, ( g–g” ) MMP13, and ( h–h” ) IL-1β indicate DQ mediates SASP in SM/J discs. Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. Distribution statistics were determined using a χ 2 test. 17 weeks old ( n DQ = 11, 6 females + 5 males; n CT = 13, 6 females + 7 males; n Nav. = 7, n Veh. = 7)

Article Snippet: Tissue sections were then blocked in 2%–10% normal serum in PBS-T, and incubated with antibodies against p19 (1:100, Novus NB200-106), p21 (1:200, Novus NB100-1941), collagen I (1:100, Abcam ab34710), aggrecan (1:50; Millipore; AB1031), chondroitin sulfate (1:300, Abcam ab11570), IL-1b (1:100, Novus NB600-633), IL-6 (1:50, Novus NB600-1131), TGFb (1:100; Abcam; ab92486), collagen X (1:500, Abcam ab58632), CA3 (1:150, Santa Cruz), and GLUT-1 (1:200, Abcam, ab40084).

Techniques: Control, Staining, Modification, Immunohistochemistry, MANN-WHITNEY

Caudal discs of SM/J mice evidence early cellular senescence and a senescence signature during degeneration. At four weeks of age, SM/J mice have increase abundance of senescence markers in their caudal discs, evidenced by ( a–a” ) p19 and ( b–b” ) p21 abundance relative to age-matched B6J discs. c Microarray analysis of 4-week-old and 17-week-old SM/J NP and AF shows distinct clustering in both tissues between the two timepoints. Thematic analysis in CompBio of enriched concepts in 17-week-old NP tissues, compared to 4-week-old tissues shows: ( d’ ) Beta-galactoside Alpha-2,3-sialytransferase Activity is an upregulated theme in the NP; ( e ) VEGF-A Complex is an upregulated theme in the AF; ( f ) CDK1 Phosphorylates Condensin is a downregulated theme in the NP; and ( g ) RUNX2 Regulates Osteoblast Differentiation is a downregulated theme in the AF. h Venn Diagram showing the gene-level overlap between SM/J tissue profiles and the SenMayo geneset, with the overlapping genes shown in ( i ). Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. n C57BL/6J 4w = 8; n SM/J 4w = 5; n SM/J 17w = 6

Journal: Bone Research

Article Title: Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice

doi: 10.1038/s41413-026-00526-4

Figure Lengend Snippet: Caudal discs of SM/J mice evidence early cellular senescence and a senescence signature during degeneration. At four weeks of age, SM/J mice have increase abundance of senescence markers in their caudal discs, evidenced by ( a–a” ) p19 and ( b–b” ) p21 abundance relative to age-matched B6J discs. c Microarray analysis of 4-week-old and 17-week-old SM/J NP and AF shows distinct clustering in both tissues between the two timepoints. Thematic analysis in CompBio of enriched concepts in 17-week-old NP tissues, compared to 4-week-old tissues shows: ( d’ ) Beta-galactoside Alpha-2,3-sialytransferase Activity is an upregulated theme in the NP; ( e ) VEGF-A Complex is an upregulated theme in the AF; ( f ) CDK1 Phosphorylates Condensin is a downregulated theme in the NP; and ( g ) RUNX2 Regulates Osteoblast Differentiation is a downregulated theme in the AF. h Venn Diagram showing the gene-level overlap between SM/J tissue profiles and the SenMayo geneset, with the overlapping genes shown in ( i ). Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. n C57BL/6J 4w = 8; n SM/J 4w = 5; n SM/J 17w = 6

Article Snippet: Tissue sections were then blocked in 2%–10% normal serum in PBS-T, and incubated with antibodies against p19 (1:100, Novus NB200-106), p21 (1:200, Novus NB100-1941), collagen I (1:100, Abcam ab34710), aggrecan (1:50; Millipore; AB1031), chondroitin sulfate (1:300, Abcam ab11570), IL-1b (1:100, Novus NB600-633), IL-6 (1:50, Novus NB600-1131), TGFb (1:100; Abcam; ab92486), collagen X (1:500, Abcam ab58632), CA3 (1:150, Santa Cruz), and GLUT-1 (1:200, Abcam, ab40084).

Techniques: Microarray, Activity Assay, MANN-WHITNEY

DQ reduces caudal disc degeneration and senescence in SM/J mice. a , b Schematic showing study design: intraperitoneal injections of DQ, Nav., or a Vehicle control were administered once every week to mice starting at 4 weeks of age and ending at 17 weeks of age. a’ –a’” SafraninO/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows DQ improves disc degeneration in SM/J mice. Images reflect the range of degenerative outcomes across treatment cohorts. b’ –b” Safranin/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows Nav. does not improve disc degeneration in SM/J mice. Quantitative immunohistochemistry shows reduced ( c–c” ) p19 (NP and AF) and ( d–d” ) p21 (AF only) in DQ-treated SM/J discs. SASP markers of ( e–e” ) TGF β, ( f–f” ) IL-6, ( g–g” ) MMP13, and ( h–h” ) IL-1β indicate DQ mediates SASP in SM/J discs. Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. Distribution statistics were determined using a χ 2 test. 17 weeks old ( n DQ = 11, 6 females + 5 males; n CT = 13, 6 females + 7 males; n Nav. = 7, n Veh. = 7)

Journal: Bone Research

Article Title: Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice

doi: 10.1038/s41413-026-00526-4

Figure Lengend Snippet: DQ reduces caudal disc degeneration and senescence in SM/J mice. a , b Schematic showing study design: intraperitoneal injections of DQ, Nav., or a Vehicle control were administered once every week to mice starting at 4 weeks of age and ending at 17 weeks of age. a’ –a’” SafraninO/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows DQ improves disc degeneration in SM/J mice. Images reflect the range of degenerative outcomes across treatment cohorts. b’ –b” Safranin/Fast Green/Hematoxylin staining evaluated with modified Thompson scoring shows Nav. does not improve disc degeneration in SM/J mice. Quantitative immunohistochemistry shows reduced ( c–c” ) p19 (NP and AF) and ( d–d” ) p21 (AF only) in DQ-treated SM/J discs. SASP markers of ( e–e” ) TGF β, ( f–f” ) IL-6, ( g–g” ) MMP13, and ( h–h” ) IL-1β indicate DQ mediates SASP in SM/J discs. Data are shown as mean ± SD. Significance was determined using an unpaired t -test or Mann-Whitney test, as appropriate. Distribution statistics were determined using a χ 2 test. 17 weeks old ( n DQ = 11, 6 females + 5 males; n CT = 13, 6 females + 7 males; n Nav. = 7, n Veh. = 7)

Article Snippet: Tissue sections were then blocked in 2%–10% normal serum in PBS-T, and incubated with antibodies against p19 (1:100, Novus NB200-106), p21 (1:200, Novus NB100-1941), collagen I (1:100, Abcam ab34710), aggrecan (1:50; Millipore; AB1031), chondroitin sulfate (1:300, Abcam ab11570), IL-1b (1:100, Novus NB600-633), IL-6 (1:50, Novus NB600-1131), TGFb (1:100; Abcam; ab92486), collagen X (1:500, Abcam ab58632), CA3 (1:150, Santa Cruz), and GLUT-1 (1:200, Abcam, ab40084).

Techniques: Control, Staining, Modification, Immunohistochemistry, MANN-WHITNEY

JUN pathway inhibition mimics the positive effect of DQ in decreasing senescence and SASP in human degenerated NP cells. a Grade IV and V human degenerated NP cells show a lower percentage of β-Gal-staining after treatment with DQ and JUN inhibitor, or only DQ, respectively. b Grade IV Human NP cells exhibit lower expression of IL-6 , MMP2 , and MMP13 compared to the stimulus group. Additionally, DQ treatment resulted in a decrease in CDKN1A and IL-6 , while T5224 enhanced MMP13 expression. c Grade V human NP cells exhibit lower expression of CDKN1A, CDKN2A, IL-6 , CCL2 , MMP2 , and MMP13 relative to the stimulus group. DQ treatment attenuated the expression of IL-6 and CCL2 , and MMP2 . T5224 ameliorated CDKN1A , IL-6 , CCL2 , and MMP2 expression. Data are shown as mean ± SD. Significance was determined using Dunnett’s multiple comparisons test ( n = 3 independent experiments, performed in triplicate)

Journal: Bone Research

Article Title: Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice

doi: 10.1038/s41413-026-00526-4

Figure Lengend Snippet: JUN pathway inhibition mimics the positive effect of DQ in decreasing senescence and SASP in human degenerated NP cells. a Grade IV and V human degenerated NP cells show a lower percentage of β-Gal-staining after treatment with DQ and JUN inhibitor, or only DQ, respectively. b Grade IV Human NP cells exhibit lower expression of IL-6 , MMP2 , and MMP13 compared to the stimulus group. Additionally, DQ treatment resulted in a decrease in CDKN1A and IL-6 , while T5224 enhanced MMP13 expression. c Grade V human NP cells exhibit lower expression of CDKN1A, CDKN2A, IL-6 , CCL2 , MMP2 , and MMP13 relative to the stimulus group. DQ treatment attenuated the expression of IL-6 and CCL2 , and MMP2 . T5224 ameliorated CDKN1A , IL-6 , CCL2 , and MMP2 expression. Data are shown as mean ± SD. Significance was determined using Dunnett’s multiple comparisons test ( n = 3 independent experiments, performed in triplicate)

Article Snippet: Tissue sections were then blocked in 2%–10% normal serum in PBS-T, and incubated with antibodies against p19 (1:100, Novus NB200-106), p21 (1:200, Novus NB100-1941), collagen I (1:100, Abcam ab34710), aggrecan (1:50; Millipore; AB1031), chondroitin sulfate (1:300, Abcam ab11570), IL-1b (1:100, Novus NB600-633), IL-6 (1:50, Novus NB600-1131), TGFb (1:100; Abcam; ab92486), collagen X (1:500, Abcam ab58632), CA3 (1:150, Santa Cruz), and GLUT-1 (1:200, Abcam, ab40084).

Techniques: Inhibition, Staining, Expressing