Journal: bioRxiv

Article Title: Discovery of CDK4-selective molecular glue degraders by high-throughput proteomics

doi: 10.64898/2026.06.19.733443

Figure Lengend Snippet: a , Proteome-wide regulations following 24 h treatment of T47D-CRBN oe cells with 1 µM NE26394 (left) or 100 nM atirmociclib (centre), and comparison of their t-statistics (right). b , Scheme for CDK4-Rb-E2F pathway. c , Expression levels of various CDK4-related proteins and protein families across seven cell lines (heatmap). Horizontal bar charts display the dependency of those cell lines on CDK4 for survival and growth (DepMap CRISPR score ; left) and the extent of downregulation induced in them by treatment with 10 µM NE26394 for 24 h (log 2 fold change; right). The treatment-associated changes in protein levels of validated target genes of E2F-induced transcription are depicted as violin plots (log 2 fold changes). Pearson correlations of protein expression levels with compound-induced depletion of CDK4 are represented below the heatmap; A negative correlation coefficient ρ suggests high protein expression associates with strong CDK4 degradation, whereas ρ ≈ 0 and ρ → 1 correspond to no and detrimental effects, respectively. * These correlations should be interpreted cautiously, as the small size of the cell line panel limits statistical robustness. d , Proteomic regulations following 24 h treatment of cell culture models of prostate cancer with 10 µM NE26394 (top) and comparison to those induced by 100 nM CDK4i atirmociclib (bottom). In the volcano plots, log 2 fold changes relative to vehicle (x-axis) and standard errors (y-axis, log 10 scale) are shown. Up-and downregulated proteins (mod. adj. p-value < 0.01) are coloured in blue and red, respectively. Non-significant (n.s.) regulations are coloured in grey. In the comparison plot, the t-statistics for regulations in two different proteomics experiments are plotted against each other. Statistically significant up- and downregulations in the x- and y-axis experiments are coloured in blue and red, respectively, overlapping significant features are coloured turquoise, and non-significant regulations are coloured grey.

Article Snippet: Atirmociclib, palbociclib and recombinant INK4A (HY-P72785) were from MedChemExpress.

Techniques: Comparison, Expressing, CRISPR, Cell Culture

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

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

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

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