Ask about this productRelated genes to: CDC27 Blocking Peptide
- Gene:
- CDC27 NIH gene
- Name:
- cell division cycle 27
- Previous symbol:
- D0S1430E, D17S978E
- Synonyms:
- APC3, ANAPC3, NUC2
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-23
- Date modifiied:
- 2017-12-06
Related products to: CDC27 Blocking Peptide
Related articles to: CDC27 Blocking Peptide
- Non-Coding regions contains genomic remnants called as Pseudogenes. For a long time, pseudogenes have been regarded as non-functional. This study investigates the previously unstudied Pseudogene CDC27P9 role in cervical cancer. Whole RNA-transcriptome profiling was performed from blood samples of n = 10 cervical cancer patients and n = 10 age matched healthy controls. CDC27P9 expression was validated in patient samples using RT-PCR. The putative CDC27P9-encoded protein structure was predicted using ChimeraX 1.9, refined predicted protein using (GROMACS 2022.2) and evaluated by Ramachandran plot. Post docking using (HADDOCK2.4) with parent gene CDC27 and other interacting genes, a 100ns MD Simulation (GROMACS 2022.2) was done. Functional studies done by siRNA-mediated silencing of CDC27P9 in HeLa cells to study Anaphase Promoting Complex/Cyclosome Pathway using RT-PCR. Cell Cycle, Mitochondrial Membrane Potential Loss and Apoptosis, using Flow Cytometry. Cell death and Chromatin Condensation was visualised using Laser Scanning Confocal Microscopy and validated in multimode microplate reader. Transcriptome sequencing revealed CDC27P9 upregulated with logFC = 10.68. RT-PCR validated overexpression of CDC27P9 in cervical cancer patients. Putative CDC27P9-encoded protein had an 93.11% of the residues point to protein structure reliability. Molecular docking and MD simulation showed strongest interactions with CDC27 and CDC20. Silencing of CDC27P9, downregulated CDC27 and Anaphase Promoting Complex/Cyclosome genes UBE2L3, PTTG1, ESPL1. In parallel downregulation of anti-apoptotic gene BCL2 while upregulation of pro-apoptotic BAX was observed. Silencing of CDC27P9 induced cell cycle arrest at S-phase, induces apoptosis and mitochondrial membrane potential loss. Observation of Condensed chromatin structure post silencing was an indicative of apoptotic signalling. Further cell death, growth inhibition and morphology changes was observed. Interestingly, silencing of CDC27P9 in cervical cancer HeLa cells caused downregulation of HPV 18. This study is the first to identify pseudogene CDC27P9 as functional with active transcripts and putative protein‑coding potential. Our findings suggest that CDC27P9 may contribute to cervical cancer progression by modulating APC/C‑mediated cell‑cycle pathways, prevent apoptosis thereby sustains cell survival in cancer cells and could be involved in HPV18-associated cellular pathways. - Source: PubMed
Publication date: 2026/03/24
Antony Edwin Rodrigues FenwickKrishnan DeenaAbbas Hussein HameedRaj Minu Jenifer MichaelSubramani SasikalaLakshman NathishJustin AntonyGovindaraj SangamiRamasamy Sivasamy - Cell division cycle 27 () gene expression is closely associated with the cell cycle and has been implicated in the pathogenesis of congenital heart disease (CHD) in animal models. This study focuses on investigating whether single-nucleotide polymorphisms (SNPs) in the gene are associated with CHD and the cardiac remodeling process in the population of Xinjiang, China. - Source: PubMed
Publication date: 2026/02/12
Yuan TengZhu FengAisan AikebaiMaheshati TunikeLi YunxiaTian RenChen You - Noncystic fibrosis (non-CF) bronchiectasis is a chronic respiratory disease characterized by irreversible bronchial dilation, with an increasing global prevalence and substantial clinical burden. Despite the advances in symptomatic management, the underlying molecular mechanisms remain poorly understood. Transcription factor DP-1 () and cell division cycle protein 27 (), which are implicated in tumorigenesis and cell cycle regulation, have not been explored in bronchiectasis. - Source: PubMed
Publication date: 2025/12/25
Hong Kang-KangLi Guo-ShengHe Rong-QuanHuang Zhi-GuangFeng Yi-ZhiKong Jin-LiangLi Lao-Dong - Oncolytic viruses (OVs) represent a promising nanomedicine strategy for cancer therapy, yet their clinical application-particularly oral administration-remains challenging due to degradation by digestive enzymes and neutralization by antibodies in the gastrointestinal tract. To address this, we developed a biomineralized cancer membrane-coated oncolytic adenovirus (CaCO@CM-OA) with enhanced resistance to enzymatic and immune clearance, significantly improving tumor-targeting efficiency. In colorectal and pancreatic cancer models, this engineered virus induced potent anti-tumor effects G2/M phase arrest, mediated by p53 phosphorylation and p21 upregulation, while suppressing epithelial-mesenchymal transition (EMT) through downregulation of N-cadherin, vimentin, and α-SMA. Furthermore, the virus triggered multimodal regulated cell death, including mitochondrial apoptosis, autophagy, and necroptosis, accompanied by immunogenic cell death (ICD) markers such as ATP release, calreticulin exposure, and HMGB1 translocation, indicating robust immune activation. Transcriptomic analysis further revealed downregulation of pro-survival genes (e.g., RHBDD2) and modulation of proliferation-related (e.g., ZMYND10, CDC27, ST7) and endocytosis-related (SNX11) genes, elucidating its multifaceted mechanism. This study highlights the potential of biomineralized OVs to overcome oral delivery barriers and enhance therapeutic efficacy in gastrointestinal cancers. By inducing synergistic cell death and immune activation, this strategy provides a foundation for clinical translation and identifies novel molecular targets for future investigation. Our findings underscore the feasibility of engineered oral OV formulations to improve treatment outcomes in intestinal malignancies. - Source: PubMed
Publication date: 2025/11/21
Hu ZujianSun YiningYu ShenleiZheng FanYan ZhuoLu NingYe LuyiYuan ShanshanZhu YutingDeng JunjieWang JilongBai Yongheng - Women are susceptible to hormonal imbalances and endocrine-related disorders such as Polycystic Ovary Syndrome (PCOS), Ovarian Cancer (OC), and Major Depressive Disorder (MDD). This study aims to identify gene-level interconnections among these conditions using omics-based bioinformatic approaches. Publicly available GEO datasets, viz., GSE226146 (PCOS), GSE18520 (OC), and GSE125664 (MDD), were analyzed, which in total resulted in 21,366 differentially expressed genes (DEGs), including 11,174 upregulated and 10,198 downregulated genes. Common genes PTTG1 and PID1 were identified using Venny 2.0. A protein-protein interaction (PPI) network was constructed using STRING, and 10 hub genes (ANAPC5, ANAPC2, PTTG1, FZR1, ANAPC4, CDC20, CDC27, ANAPC10, UBE2C, and BUB1) were identified using CytoHubba based on MCC scoring. Functional enrichment analysis showed significant involvement of these genes in oocyte meiosis, progesterone-mediated oocyte maturation, mitotic regulation, and metaphase-anaphase transition (p < 0.05). PTTG1, identified as both a common and hub gene, was downregulated in PCOS and upregulated in OC and MDD. Drug-gene interaction analysis using DSigDB via Enrichr identified Alvespimycin (for PCOS) and Gefitinib (for OC) as drugs targeting PTTG1. Molecular docking using AutoDock 4.2.6 showed that Alvespimycin and Ephedrone bind PTTG1 with a binding affinity of - 4.59 kcal/mol and - 5.81 kcal/mol, respectively, while Gefitinib showed - 4.92 kcal/mol, slightly less than Troglitazone (-5.3 kcal/mol) for OC. This study highlights PTTG1 as a shared molecular link among PCOS, OC, and MDD, suggesting its potential as a therapeutic target and providing insights into the genetic and physiological overlap of these conditions. - Source: PubMed
Publication date: 2025/09/05
Kumari KavitaSingh AakanshaDwivedi Anjana