ArticleOncogene2018
Hic-5 regulates fibrillar adhesion formation to control tumor extracellular matrix remodeling through interaction with tensin1.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 39 citations in OpenAlex.
- Substrate curvature and stiffness equivalence in governing cell mechanosensing.Nature communications · 2026Article
- Fibrillar adhesion dynamics govern the timescales of nuclear mechano-response via the vimentin cytoskeleton.Nature materials · 2026Article
- Hic-5 promotes the progression of nonalcoholic steatohepatitis by regulating hepatocellular fatty acid metabolism through the PTEN/PGE2/EP4 axis.Molecular biomedicine · 2026Article
- Hic-5 deficiency attenuates MAFLD by inhibiting neutrophils migration via the CXCL1-CXCR2 axis.Journal of gastroenterology · 2025Article
- Tensins in Cancer: Integration of Their Domain Functions, Context-Dependent Regulation and Biomarker Potential.Biology · 2025Review
- A comparative analysis of paxillin and Hic-5 proximity interactomes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Fibroblast integrin α11β1 is a collagen assembly receptor in mechanoregulated fibrillar adhesions.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Hic-5 regulates extracellular matrix-associated gene expression and cytokine secretion in cancer associated fibroblasts.Experimental cell research · 2024Article
- Forces exerted and transduced by cancer-associated fibroblasts during cancer progression.Biology of the cell · 2023Review
- Tensins in Kidney Function and Diseases.Life (Basel, Switzerland) · 2023Review
- Deciphering the Kidney Matrisome: Identification and Quantification of Renal Extracellular Matrix Proteins in Healthy Mice.International journal of molecular sciences · 2023Article
- Identification of the hub genes associated with prostate cancer tumorigenesis.Frontiers in oncology · 2023Article
- Integrin α11β1 in tumor fibrosis: more than just another cancer-associated fibroblast biomarker?Journal of cell communication and signaling · 2022Review
- Physiological and pathological roles of Hic‑5 in several organs (Review).International journal of molecular medicine · 2022Review
- Review
- Tensin3 interaction with talin drives the formation of fibronectin-associated fibrillar adhesions.The Journal of cell biology · 2022Article
- Review
- Tensins - emerging insights into their domain functions, biological roles and disease relevance.Journal of cell science · 2021Review
- Actin dynamics during tumor cell dissemination.International review of cell and molecular biology · 2021Review
- Hic-5 is required for activation of pancreatic stellate cells and development of pancreatic fibrosis in chronic pancreatitis.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The linearization of the stromal extracellular matrix (ECM) by cancer-associated fibroblasts (CAFs) facilitates tumor cell growth and metastasis. However, the mechanism by which the ECM is remodeled is not fully understood. Hic-5 (TGFβ1i1), a focal adhesion scaffold protein, has previously been reported to be crucial for stromal ECM deposition and remodeling in vivo. Herein we show that CAFs lacking Hic-5 exhibit a significant reduction in the ability to form fibrillar adhesions, a specialized form of focal adhesion that promote fibronectin fibrillogenesis. Hic-5 was found to promote fibrillar adhesion formation through a newly characterized interaction with tensin1. Furthermore, Src-dependent phosphorylation of Hic-5 facilitated the interaction with tensin1 to prevent β1 integrin internalization and trafficking to the lysosome. The interaction between Hic-5 and tensin1 was mechanosensitive, promoting fibrillar adhesion formation and fibronectin fibrillogenesis in a rigidity-dependent fashion. Importantly, this Src-dependent mechanism was conserved in three-dimensional (3D) ECM environments. Immunohistochemistry of tensin1 showed enrichment in CAFs in vivo, which was abrogated upon deletion of Hic-5. Interestingly, elevated Hic-5 expression correlates with reduced distant metastasis-free survival in patients with basal-like, HER2+ and grade 3 tumors. Thus, we have identified Hic-5 as a crucial regulator of ECM remodeling in CAFs by promoting fibrillar adhesion formation through a novel interaction with tensin1.
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.