AI Article Synopsis
- Understanding organ size control is crucial in biology, as improper growth regulation can lead to tumor formation.
- The Hippo signaling pathway is a key player in growth regulation and has roles in cancer, acting through specific miRNAs to influence cell proliferation and apoptosis.
- This study identifies the gene Tribbles as a direct target that limits cell proliferation by suppressing the G2/M transition, highlighting its central role in tissue growth and tumorigenesis, alongside other cell cycle regulators.
Article Abstract
One of the fundamental issues in biology is understanding how organ size is controlled. Tissue growth has to be carefully regulated to generate well-functioning organs, and defects in growth control can result in tumor formation. The Hippo signaling pathway is a universal growth regulator and has been implicated in cancer. In , the Hippo pathway acts through the miRNA to regulate cell proliferation and apoptosis. Even though the targets regulating apoptosis have been determined, the target genes controlling proliferation have not been identified thus far. In this study, we identify the gene as a direct target gene. Tribbles limits cell proliferation by suppressing G2/M transition. We show that regulation by is central in controlling tissue growth and tumorigenesis. We expand our study to other cell cycle regulators and show that deregulated G2/M transition can collaborate with oncogene activation driving tumor formation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6653758 | PMC |
| http://dx.doi.org/10.26508/lsa.201900381 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Metabolic Signaling in the Tumor Microenvironment.
Cancers (Basel)
January 2025
Department of Molecular Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Cancer cells must reprogram their metabolism to sustain rapid growth. This is accomplished in part by switching to aerobic glycolysis, uncoupling glucose from mitochondrial metabolism, and performing anaplerosis via alternative carbon sources to replenish intermediates of the tricarboxylic acid (TCA) cycle and sustain oxidative phosphorylation (OXPHOS). While this metabolic program produces adequate biosynthetic intermediates, reducing agents, ATP, and epigenetic remodeling cofactors necessary to sustain growth, it also produces large amounts of byproducts that can generate a hostile tumor microenvironment (TME) characterized by low pH, redox stress, and poor oxygenation.
View Article and Find Full Text PDFPRMT5 inhibition has a potent anti-tumor activity against adenoid cystic carcinoma of salivary glands.
J Exp Clin Cancer Res
January 2025
Department of Medicine, Section of Hematology and Oncology, University of Chicago, Chicago, IL, USA.
Background: Adenoid cystic carcinoma (ACC) is a rare glandular malignancy, commonly originating in salivary glands of the head and neck. Given its protracted growth, ACC is usually diagnosed in advanced stage. Treatment of ACC is limited to surgery and/or adjuvant radiotherapy, which often fails to prevent disease recurrence, and no FDA-approved targeted therapies are currently available.
View Article and Find Full Text PDFInactivation of TACC2 epigenetically represses CDKN1A and confers sensitivity to CDK inhibitors.
Med
January 2025
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, P.R. China. Electronic address:
Background: The genomic landscape of esophageal squamous cell carcinoma (ESCC) has been characterized extensively, but there remains a significant need for actionable targets and effective therapies.
Methods: Here, we perform integrative analysis of genome-wide loss of heterozygosity and expression to identify potential tumor suppressor genes. The functions and mechanisms of one of the candidates, TACC2, are then explored both in vitro and in vivo, leading to the proposal of a therapeutic strategy based on the concept of synthetic lethality.
Noncanonical UPR factor CREB3L2 drives immune evasion of triple-negative breast cancer through Hedgehog pathway modulation in T cells.
Sci Adv
January 2025
Zhejiang Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang Key Laboratory of Frontier Medical Research on Cancer Metabolism, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou, China.
The unfolded protein response (UPR) pathway is crucial for tumorigenesis, mainly by regulating cancer cell stress responses and survival. However, whether UPR factors facilitate cell-cell communication between cancer cells and immune cells to drive cancer progression remains unclear. We found that adenosine 3',5'-monophosphate response element-binding protein 3-like protein 2 (CREB3L2), a noncanonical UPR factor, is overexpressed and activated in triple-negative breast cancer, where its cleavage releases a C-terminal fragment that activates the Hedgehog pathway in neighboring CD8+ T cells.
View Article and Find Full Text PDFA multidimensional pan-cancer analysis of NDUFA4L2 and verification of the oncogenic value in colon cancer.
FASEB J
January 2025
Department of General Surgery, Sir Run Run Hospital of Nanjing Medical University, Nanjing, Jiangsu, P. R. China.
NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) protein is located in the mitochondria and can regulate cell proliferation. Some studies have shown that the high NDUFA4L2 expression is linked with poor prognosis and cancer progression in various patients with cancers. However, the correlation between NDUFA4L2 and pan-cancer is unknown.
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!