ReviewCarcinogenesis2022
Unravelling the distinct biological functions and potential therapeutic applications of TIMP2 in cancer.
Review in Carcinogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- ADAM and ADAMTS proteases as integrative hubs in heart failure pathogenesis and therapy.iScience · 2026Review
- AdipoRon Modulation of the Invasive Potential of Prostate Cancer Cells Is Dependent on Their EMT-Related Phenotype.Biomedicines · 2026Article
- Extracellular matrix and proteolysis: mechanisms driving irreversible changes and shaping cell behavior.The FEBS journal · 2026Review
- When proteases reshape barriers: Basement membrane remodelling in development, wound healing and tumour progression.The FEBS journal · 2026Review
- Extracellular vesicles delivering TIMP-2 modulate MMP-1, MMP-2, and MMP-9 expression in human lung adenocarcinoma A549 cells.Frontiers in pharmacology · 2026Article
- Brain-rejuvenating factor TIMP2 is associated with brain health and neuroprotective lifestyle in aged subjects.medRxiv : the preprint server for health sciences · 2025Article
- Extracellular Matrix (ECM)-Regulated Molecular Switches: Tissue Inhibitors of Metalloproteinases in Synaptic Formation and Neuropathic Diseases.Cellular and molecular neurobiology · 2025Review
- Histidine Tag-Specific PEGylation Improves the Circulating Half-Life of TIMP2.ACS applied bio materials · 2025Article
- miRNA-503 inhibition exerts anticancer effects and reduces tumor growth in mesothelioma.Journal of experimental & clinical cancer research : CR · 2025Article
- Dietary Arginine Supplementation Modulates the Proteome of Boar Seminal Plasma.Animals : an open access journal from MDPI · 2025Article
- Diamond Nanoparticles Suppress Migration of T98G Glioblastoma Cells by Targeting ECM-Integrin Interactions and Intracellular Signaling, Leading to Extensive Proteome Alterations.Nanotechnology, science and applications · 2025Article
- Assessing Gelatinase Activity in Normal and Disease Uterine Tissue and Cells Via Gelatin Zymography.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Epigenomic and phenotypic characterization of DEGCAGS syndrome.European journal of human genetics : EJHG · 2024Article
- Mapping Extracellular Protein-Protein Interactions Using Extracellular Proximity Labeling (ePL).Journal of proteome research · 2024Article
- MicroRNA 429 regulates MMPs expression by modulating TIMP2 expression in colon cancer cells and inflammatory colitis.Genes & genomics · 2024Article
- Circular RNA circLIFR suppresses papillary thyroid cancer progression by modulating the miR-429/TIMP2 axis.Journal of cancer research and clinical oncology · 2024Article
- Article
- Characterization of Angiogenic, Matrix Remodeling, and Antimicrobial Factors in Preterm and Full-Term Human Umbilical Cords.Journal of developmental biology · 2024Article
- The TIMP protein family: diverse roles in pathophysiology.American journal of physiology. Cell physiology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Tissue inhibitors of metalloproteinases (TIMPs) are a conserved family of proteins that were originally identified as endogenous inhibitors of matrixin and adamalysin endopeptidase activity. The matrixins and adamalysins are the major mediators of extracellular matrix (ECM) turnover, thus making TIMPs important regulators of ECM structure and composition. Despite their high sequence identity and relative redundancy in inhibitory profiles, each TIMP possesses unique biological characteristics that are independent of their regulation of metalloproteinase activity. As our understanding of TIMP biology has evolved, distinct roles have been assigned to individual TIMPs in cancer progression. In this respect, data regarding TIMP2's role in cancer have borne conflicting reports of both tumor suppressor and, to a lesser extent, tumor promoter functions. TIMP2 is the most abundant TIMP family member, prevalent in normal and diseased mammalian tissues as a constitutively expressed protein. Despite its apparent stable expression, recent work highlights how TIMP2 is a cell stress-induced gene product and that its biological activity can be dictated by extracellular posttranslational modifications. Hence an understanding of TIMP2 molecular targets, and how its biological functions evolve in the progressing tumor microenvironment may reveal new therapeutic opportunities. In this review, we discuss the continually evolving functions of TIMP proteins, future perspectives in TIMP research, and the therapeutic utility of this family, with a particular focus on TIMP2.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.