AI Article Synopsis
- p31(Comet) is a key player in the spindle assembly checkpoint (SAC) and helps promote mitotic exit by inhibiting Mad2, although how it's regulated is not well understood.
- The Rb-E2F pathway controls the expression of p31(Comet), and its levels are found to increase alongside Mad2 in various tumors, such as breast and lung cancers.
- Proper balance between p31(Comet) and Mad2 is crucial for cell viability, and imbalances may contribute to chromosomal instability and tumor development.
Article Abstract
p31(Comet) is a well-known interacting partner of the spindle assembly checkpoint (SAC) effector molecule Mad2. At the molecular level it is well established that p31(Comet) promotes efficient mitotic exit, specifically the metaphase-anaphase transition, by antagonizing Mad2 function. However, there is little knowledge of how p31(Comet) is regulated or the physiological importance of controlling p31(Comet). Here, we show that the Rb-E2F pathway regulates p31(Comet) expression. In multiple tumor types (including breast and lung) p31(Comet) expression is increased along with Mad2. Expression of this antagonist-target pair is coordinated in cells and correlated in cancer. Moreover, a narrow range of p31(Comet):Mad2 ratios is compatible with cellular viability. Our data suggest that coordinate regulation is important for the outgrowth of oncogenic cell populations. Our findings suggest that altered p31(Comet):Mad2 expression ratios may provide new insight into altered SAC function and the generation of chromosomal instability in tumors.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3905074 | PMC |
| http://dx.doi.org/10.4161/cc.26811 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Prolonged cell cycle arrest in response to DNA damage in yeast requires the maintenance of DNA damage signaling and the spindle assembly checkpoint.
Elife
December 2024
Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.
Cells evoke the DNA damage checkpoint (DDC) to inhibit mitosis in the presence of DNA double-strand breaks (DSBs) to allow more time for DNA repair. In budding yeast, a single irreparable DSB is sufficient to activate the DDC and induce cell cycle arrest prior to anaphase for about 12-15 hr, after which cells 'adapt' to the damage by extinguishing the DDC and resuming the cell cycle. While activation of the DNA damage-dependent cell cycle arrest is well understood, how it is maintained remains unclear.
View Article and Find Full Text PDFMitotic Arrest Deficient 2 Like 1 Contributes to Colorectal Cancer Cell Migration, Invasion, and Oxaliplatin Resistance Through the Wnt/β-Catenin Pathway.
Chem Biol Drug Des
November 2024
Department of Gastrointestinal Surgery, Yueyang Central Hospital, Yueyang, Hunan, People's Republic of China.
Colorectal cancer (CRC) is a highly prevalent malignancy, requiring chemotherapy for advanced stages of the disease. Previously, we found that mitotic arrest deficient 2 like 1 (MAD2L1) was upregulated and facilitated malignant proliferation in CRC. However, the association between MAD2L1 expression and tumor progression, as well as chemotherapy resistance in CRC, remains unclear.
View Article and Find Full Text PDFUnveiling novel prognostic biomarkers and therapeutic targets for HBV-associated hepatocellular carcinoma through integrated bioinformatic analysis.
Medicine (Baltimore)
October 2024
Medical Laboratory Center, Xi'an TCM Hospital of Encephalopathy, Xi'an, China.
Article Synopsis
- Hepatocellular carcinoma (HCC) is a major cancer threat worldwide with few treatment options, prompting research into prognosis and therapy for patients with hepatitis B (HBV)-related HCC.
- The study analyzed data from three microarray datasets, uncovering 374 differentially expressed genes, including significant hub genes linked to poor patient prognosis.
- Key genes like ZWINT and CDK1 were identified as potential biomarkers, suggesting they could help predict disease progression and guide new treatment approaches, while further research is needed on other hub genes.
Targeting KIFC1 Promotes Senescence in Soft Tissue Sarcoma via FXR1-Dependent Regulation of MAD2L1 mRNA Stability.
Adv Sci (Weinh)
November 2024
Melanoma and Sarcoma Medical Oncology Unit, Sun Yat-sen University Cancer Center, Guangzhou, Guangdong, 510060, P. R. China.
Patients diagnosed with soft tissue sarcoma (STS) often present at intermediate to advanced stages, with inherently limited therapeutic options available. There is an urgent need to identify novel therapeutic targets. In this study, by screening STS data from the Cancer Genome Atlas (TCGA) and Genotype Tissue Expression (GTEx) databases, KIFC1 is identified as a potential biomarker and a promising therapeutic target for STS.
View Article and Find Full Text PDFHNRNPD/MAD2L2 axis facilitates lung adenocarcinoma progression and is a potential prognostic biomarker.
Cell Signal
December 2024
Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou 450052, China. Electronic address:
Background: Although progress has been made in the treatment of LAUD, the survival rate for patients remains poor. An in-depth grasp of the molecular pathways implicated in LUAD progression is vital for improving diagnosis and treatment strategies. This study aims to explore novel molecular mechanisms driving LUAD progression and identify new potential prognostic biomarkers for LAUD patients.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!