Journal: Cell Death & Disease

Article Title: Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma

doi: 10.1038/s41419-026-08593-5

Figure Lengend Snippet: A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Article Snippet: The primary antibodies used were as follows: PI3K p110δ (A19742; ABclonal), pan-Akt (#4691; CST), phospho-Akt (Ser473, #4060; CST), PPARα (ab227074; Abcam), FoxO1 (#2880; CST), phospho-FoxO1 (Thr24, #9464; CST) and (Ser256, #9461; CST), FoxO3a (#12829; CST), FoxO4 (#9472; CST), Mcl-1 (#16225-1-AP; Proteintech), Bcl-2 (#12789-1-AP; Proteintech), Bim (A19702; ABclonal), Bax (#50599-2-Ig; Proteintech), Cleaved PARP(#5625; CST), P21(#2947; CST), p27 (#3686; CST), Cyclin E1 (#11935-1-AP; Proteintech), CDK2 (#10122-1-AP; Proteintech), phospho-CDK2 (#4539; CST), GLUT1(#73015; CST), PGK1(A12686; ABclonal), β-Tubulin (#10094-1-AP; Proteintech), Lamin B1 (#13435; CST), and β-Actin (#66009-1-Ig; Proteintech).

Techniques: DNA Synthesis, Staining, Western Blot

Journal: Journal of Biological Chemistry

Article Title: Glypican-1 Stimulates Skp2 Autoinduction Loop and G1/S Transition in Endothelial Cells

doi: 10.1074/jbc.m111.325282

Figure Lengend Snippet: FIGURE 4. GPC1 up-regulates CDK2 and down-regulates p21Cip1 and p27Kip1. A and B, mouse brain ECs were transduced with different doses of control or GPC1 adenovirus for 48 h, and the protein levels of CDK2, p21, and p27 as well as p57 were determined by immunoblot analysis, with -actin as loading control. C, quantitative RT-PCR. Total RNAs were isolated from the mouse brain ECs treated with 10 MOI of control or GPC1 adenovirus for 48 h. Relative mRNA levels of different genes comparing GPC1 and control adeno- virus-treated cells were measured by quantitative RT-PCR. Each bar repre- sents the mean S.E. of three independent experiments. *The mRNA level of p21 was significantly down-regulated by GPC1 (p 0.05).

Article Snippet: Reagents and Plasmids—Antibodies to cyclins D1, D2, D3, A, andB1, p16, p18, p19, p21, p27, p57, CDK4, CDK6, CDK2, Skp2 and Id1 were from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Transduction, Control, Western Blot, Quantitative RT-PCR, Isolation, Virus

Journal: Journal of Biological Chemistry

Article Title: Glypican-1 Stimulates Skp2 Autoinduction Loop and G1/S Transition in Endothelial Cells

doi: 10.1074/jbc.m111.325282

Figure Lengend Snippet: FIGURE 10. Schematic of GPC1 stimulation of G1-S cell cycle progression byactivatingtheSkp2autoinductionloop.TheSkp2autoinductionloop,a positive feedback mechanism during E2F activation, is comprised of pRb-E2F, Skp2, p27/p21, and cyclin E/A-CDK2. Cellular alterations that directly or indi- rectly activate the loop may lead to mitogen-independent S phase entry or acceleration of ongoing G1-S progression. Our findings are consistent with GPC1-induced G1-S progression via activation of the Skp2 autoinduction loop,independentlyofcyclinD-CDK4/6.c-Myc,whichcanbeup-regulatedby GPC1-stimulated MAPK and Wnt signaling, is a likely intermediate effector. c-Myc targets both p21 and D cyclins for transcriptional repression. Down- regulation of p21 expression appears, at least partially, to contribute to the GPC1-induced activation of the Skp2 autoinduction loop.

Article Snippet: Reagents and Plasmids—Antibodies to cyclins D1, D2, D3, A, andB1, p16, p18, p19, p21, p27, p57, CDK4, CDK6, CDK2, Skp2 and Id1 were from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Activation Assay, Expressing

Journal: Cancer cell

Article Title: Long-term breast cancer response to CDK4/6 inhibition defined by TP53-mediated geroconversion

doi: 10.1016/j.ccell.2024.09.009

Figure Lengend Snippet: (A) Sample collection in FELINE trial. Core needle biopsy was performed over the course of treatment: screening (day 0), cycle 1 (day 14), and end of treatment (day 180). (B) Ki-67 trend is depicted for all patients in the FELINE trial for whom Ki-67 was evaluable at all time points and sequencing of the day 0 tumor was performed. The rates of Ki-67 > 10% at surgery are compared by pre-treatment TP53 status utilizing Fisher’s exact (two-sided) test. (C) Proliferation score in wild type and mutant TP53 tumors at baseline, on-treatment day14 and EOT. (D and F) GSEA of DREAM complex genes in WT compared vs. MT at day14 (left) and EOT (right). (E) GSEA of senescence ribo genes. EOT vs. baseline in WT TP53 (left) and in MT (right) (F) Model for loss of p53 resistant mechanism. In the presence of p53, CDK4/6i inhibited phosphorylation of RB and p130. The cells were arrested in quiescence through DREAM complex, leading to irreversible cell-cycle arrest. Loss-of-function p53 and insufficient p21 enabled CDK2 to retain phosphorylated p130, leading to cell-cycle re-entry and escape from quiescence. See also .

Article Snippet: CDK2 , Cell Signaling Technology , 2546S, RRID: AB_10695594.

Techniques: Sequencing, Mutagenesis, Phospho-proteomics

Journal: Biochemistry and Biophysics Reports

Article Title: miR-21-5p inhibitor enhances the radiosensitivity of human cervical cancer cells via blocking CPEB3-mediated CDK1/cyclin B pathway

doi: 10.1016/j.bbrep.2025.102177

Figure Lengend Snippet: miR-21-5p inhibitor directly targeting CPEB3-mediated suppression of CDK1/cyclin B. (A) Bioinformatics analysis revealed the predicted binding sites between miR-21-5p and CPEB3; (B) Effect of miR-21-5p on mRNA expression level of CPEB3 in human cervical cancer cells. HeLa or SiHa cells were transfected with miR-21-5p for 48 h, the mRNA expression level of CPEB3 was determined by RT-PCR; (C) Luciferase reporter assay was performed to measure the binding activity and key binding sites between CPEB3 and miR-21-5p; (D) Effect of miR-21-5p on the expression of CPEB3-mediated CDK1/cyclin B. HeLa or SiHa cells were treated by miR-21-5p inhibitor for 48 h, the expression of CPEB3, CDK1, Cyclin B and β-actin were determined by immunoblot analysis; ∗∗p < 0.01.

Article Snippet: The information of primary antibodies as follow CDK1 (CST #18048), cyclin B (CST # #12231), β-actin (CST #3700), CPEB3 (Invitrogen #12669-1-AP).

Techniques: Binding Assay, Expressing, Transfection, Reverse Transcription Polymerase Chain Reaction, Luciferase, Reporter Assay, Activity Assay, Western Blot