CDKN1A Antibody
- Known as:
- CDKN1A Antibody
- Catalog number:
- XW-7422
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- CDKN1A Antibody
Related genes to: CDKN1A Antibody
- Gene:
- CDKN1A NIH gene
- Name:
- cyclin dependent kinase inhibitor 1A
- Previous symbol:
- CDKN1
- Synonyms:
- P21, CIP1, WAF1, SDI1, CAP20, p21CIP1, p21Cip1/Waf1, p21
- Chromosome:
- 6p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-24
- Date modifiied:
- 2018-06-06
Related products to: CDKN1A Antibody
Related articles to: CDKN1A Antibody
- Selective targeting of cancer cells is a critical strategy in anticancer therapy, and the overexpression of glucose transporters (GLUTs) in malignant cells provides an attractive avenue for achieving this selectivity. In this study, we report the synthesis and biological evaluation of glycoconjugate vanadyl complexes as GLUT-directed anticancer agents against breast cancer. A Schiff base ligand (CG) was synthesized through the condensation of curcumin (C) and glucosamine (G), followed by complexation with vanadyl to form [VO(CG)₂]·5H₂O. The synthesized compounds were comprehensively characterized by elemental analysis, MS, NMR, FT-IR, TGA, molar conductance, and magnetic susceptibility measurements. Spectroscopic and computational studies confirmed that the ligand coordinates in a bidentate chelating mode via the azomethine nitrogen and the enolic oxygen. Biological evaluation in MCF-7 breast cancer cells included cytotoxicity assays, molecular docking, DNA-binding studies, and quantitative gene expression analysis. Both compounds exhibited cytotoxic activity, with the CG ligand showing the highest potency (IC₅₀ = 7.51 ± 0.12 μg/mL or 14.2 μM). Notably, co-treatment with the GLUT inhibitor quercetin significantly increased the IC₅₀ value, suggesting the involvement of GLUT-mediated cellular uptake. Molecular docking studies indicated favorable binding affinity toward GLUT, while DNA-binding experiments demonstrated interaction with DNA. Treatment of MCF-7 cells with the glycoconjugate ligand induced DNA damage, modulated the expression of cell cycle- and apoptosis-related genes, and promoted apoptosis. Flow cytometric analysis demonstrated that the glycoconjugate significantly arrested MCF-7 cells in the S-phase (49.40% vs 22.22% in control). This finding is consistent with impaired cell cycle progression and may be associated with the observed DNA interaction. Quantitative real-time PCR analysis of the CG compound revealed significant upregulation of BAX and CDKN1A (p21) (p ≤ 0.05) and pronounced upregulation of STK11 (LKB1) (p ≤ 0.001), suggesting activation of the AMPK signaling pathway and a metabolic stress response. Overall, the glycoconjugate ligand induces apoptosis and cell cycle arrest through oxidative and metabolic stress mediated by AMPK-STK11 signaling, highlighting its potential as a GLUT-targeted chemotherapeutic agent for breast cancer treatment. - Source: PubMed
Publication date: 2026/08/14
Hassan Safaa SRashidi Fatma BSeddik Ramy GEl-Sayed Areej WMohamed Habiba AMohamed Hager WKenawy Menna MHussein Nouran BAfify Nourhan AMegahed Noura MZeinhom Reem MAbdultawab Ziad AElgohary AyatallahHamido NashwaElwakil Ahmed IAlzoghaly Hadeel ANabil Martina OAhmed Ehab AIsmail Khaled M - Within an integrative medicine approach that links veterinary and human health, red algae extracts are gaining attention as promising sources of natural bioactive compounds with potential anticancer properties. This study investigates the selectivity of extract (PCE) against canine cancer cell lines and its transcriptional effects in C2 canine mastocytoma cells. - Source: PubMed
Publication date: 2026/07/30
Maghrebi HananeMucignat GretaLakhdar FatimaBenhniya BouchraDi Paolo VeronicaEtahiri SamiraCapolongo FrancescaPauletto MariannaGiantin MeryDacasto Mauro - To investigate the expression and function of Zeste 12 homolog (SUZ12) in hepatocellular carcinoma (HCC), and to preliminarily explore its biological role and underlying molecular mechanisms in HCC. This cell-based experimental study was conducted at the Basic Laboratory of the General Hospital of Southern Theater Command of the PLA from June 2024 to June 2025. The mRNA and protein expression levels of SUZ12 in HCC tissues and their correlations with clinicopathological features were analyzed using The Cancer Genome Atlas (TCGA). The prognostic impact of SUZ12 on HCC patients was evaluated using the K-M plotter database. SUZ12 overexpression and knockdown models were established in human hepatocellular carcinoma cells (HepG2). Transfection efficiency was verified by quantitative real-time polymerase chain reaction (qPCR) and Western blot. The effects of SUZ12 on HCC cell proliferation, invasion, and migration were assessed via Cell Counting Kit-8 assay (CCK-8), colony formation assay, and Transwell assay. The interaction between SUZ12 and enhancer of Zeste homolog 2 (EZH2) was validated by Co-Immunoprecipitation (Co-IP). Western blot was further used to preliminarily examine the effects of SUZ12 on the protein expression levels of H3K27me3 and CDKN1A. Statistical analyses were performed using two independent-sample t-tests In HCC tissues, SUZ12 mRNA levels were significantly higher than those in normal liver tissues (TPM=7.644 . 4.643, =-6.648, <0.001), and SUZ12 protein expression levels were also significantly elevated (Z-score=0.004 .-1.621, =-9.815, <0.001). The mRNA expression level of SUZ12 showed an increasing trend with higher clinical stage (normal: 4.643; stage Ⅰ: 7.071; stage Ⅱ: 7.085; stage Ⅲ: 8.677 TPM,=36.700, <0.001) and pathological grade (normal: 4.643; grade 1: 5.589; grade 2: 7.032; grade 3: 8.586 TPM, =38.200, <0.001). In the CCK-8 assay, the cell viability value in the SUZ12 overexpression group was higher than that in the control group; the relative absorbance at 450 nm on day 1(0.370±0.020 . 0.379±0.010, =0.376, =0.725), day 2 (0.477±0.016 . 0.370±0.069, =-4.391, =0.005), day 3 (0.900±0.022 . 0.816±0.024, =-6.577, =0.001), day 4 (1.601±0.017 . 1.390±0.026, =-2.477, =0.048). The cell viability value in the SUZ12 knockdown group was lower than that in the control group; the relative absorbance at 450 nm on day 1 (0.277±0.005 . 0.287±0.001, =1.737, =0.133), day 2 (0.344±0.002 . 0.377±0.006, =4.677, =0.010), day 3 (0.643±0.006 . 0.720±0.006, =4.142, =0.012), day 4 (1.065±0.015 . 1.210±0.031, =8.941, <0.001). In the colony formation assay, the number of colonies formed in the SUZ12 overexpression group was significantly higher than that in the control group [(775.000±51.884) colonies . (429.333±16.756 )colonies, =-6.340, =0.003]; the number of colonies decreased in the knockdown group [(150.666±4.055) colonies . (272.666±7.172) colonies, =13.917, <0.001]. In the Transwell assay, the invasion ability [(329.000±33.291) cells . (229.333±12.732) cells, =-4.564, =0.010] and migration ability [(325.333±7.310) cells . (217.333±1.732) cells, =-14.120, <0.001)] were significantly enhanced in the SUZ12 overexpression group compared to the control group; the invasion ability [(269.000±19.467) cells . (374.000±22.500) cells, =3.529, =0.024] and migration ability [(163.333±8.412) cells . (272.333±19.220) cells, =6.194, =0.020] were significantly weakened in the SUZ12 knockdown group compared to the control group. Western blot results suggested that high expression of SUZ12 downregulated the protein expression level of CDKN1A. SUZ12 high expression is associated with malignant biological behaviors of HCC cells. The SUZ12/EZH2/CDKN1A axis may represent a potential therapeutic target for patients with advanced HCC. - Source: PubMed
Xuan J FMa L YGuo R XLi W QZhang W YSun Z H - This study aimed to identify and prioritize gut microbiota-derived metabolite-associated host candidate targets in high-risk primary biliary cholangitis (PBC) through integrative multi-omics analysis and external validation. - Source: PubMed
Publication date: 2026/08/13
Feng JingLiu ZhiyunSun Huanna - Cervical carcinoma is predominantly driven by high-risk human papillomavirus (HPV) infection, in which functional inactivation of p53 occurs mainly through viral oncoproteins rather than mutations in the gene. This raises questions concerning the prognostic relevance of gene status and p53 protein levels in this tumor type. This study aimed to systematically evaluate the prognostic significance of mutation status, p53 protein abundance, and selected downstream p53-regulated proteins in cervical carcinoma, with particular focus on tumors carrying wild-type . Clinical and proteomic data from 162 cervical carcinoma patients were retrieved from The Cancer Genome Atlas (TCGA). Protein levels (p53, BAX, p21/CDKN1A, and TIGAR) were assessed using reverse-phase protein array (RPPA) data. Survival analyses were performed using Kaplan-Meier estimates with log-rank testing after stratification into quartile-based expression groups. The vast majority of tumors (~93%) harbored wild-type , and the mutation status showed no association with patient survival. In tumors with wild-type , p53 protein levels did not significantly correlate with overall survival, indicating a limited prognostic value. In contrast, elevated levels of the pro-apoptotic protein BAX showed a clear tendency to be associated with poorer overall and progression-free survival, suggesting BAX as a potential prognostic marker in this specific molecular context. The expression of p21/ showed no prognostic relevance, while high TIGAR levels displayed a slight trend toward poorer survival, although without reaching statistical significance. In summary, in HPV-driven cervical carcinoma, neither the mutation status nor the p53 protein abundance reliably predict patient outcome. Instead, selected downstream effectors of p53 signaling-particularly BAX-may provide more informative prognostic insights in tumors retaining wild-type . These findings highlight the importance of assessing functional outputs of p53 signaling rather than the p53 status alone in this disease context. - Source: PubMed
Publication date: 2026/07/27
Toennießen-Klein Sebastian MRangno DennisSunil AbhiramiBozko MariaBozko Przemyslaw