ArticleCancer research2014
CD98hc (SLC3A2) loss protects against ras-driven tumorigenesis by modulating integrin-mediated mechanotransduction.
Article in Cancer research, 2014. 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
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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.
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Who cites it
35 citing papers in PubMed, 76 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- ERα36 is associated with SLC7A5/LAT1 expression, cervical cancer progression, and BNCT response: a translational study.Frontiers in oncology · 2026Article
- Amino acid transporters within the solute carrier superfamily: Underappreciated proteins and novel opportunities for cancer therapy.Molecular metabolism · 2024Review
- Matrix stiffness-driven cancer progression and the targeted therapeutic strategy.Mechanobiology in medicine · 2023Review
- CD98 heavy chain as a prognostic biomarker and target for cancer treatment.Frontiers in oncology · 2023Review
- Matrix stiffness-dependent STEAP3 coordinated with PD-L2 identify tumor responding to sorafenib treatment in hepatocellular carcinoma.Cancer cell international · 2022Article
- Oncogenic RAS commandeers amino acid sensing machinery to aberrantly activate mTORC1 in multiple myeloma.Nature communications · 2022Article
- N-glycosylation is crucial for trafficking and stability of SLC3A2 (CD98).Scientific reports · 2022Article
- Increased/Targeted Brain (Pro)Drug Delivery via Utilization of Solute Carriers (SLCs).Pharmaceutics · 2022Review
- Feature selection and classification over the network with missing node observations.Statistics in medicine · 2022Article
- CD98hc has a pivotal role in maintaining the immuno-barrier integrity of basal layer cells in esophageal epithelium.Cancer cell international · 2022Article
- Matrix Stiffness Contributes to Cancer Progression by Regulating Transcription Factors.Cancers · 2022Review
- Ferroptosis: A Specific Vulnerability of RAS-Driven Cancers?Frontiers in oncology · 2022Article
- Expression of CD98hc in Pancreatic Cancer and Its Role in Cancer Cell Behavior.Journal of Cancer · 2022Article
- Cellular feedback dynamics and multilevel regulation driven by the hippo pathway.Biochemical Society transactions · 2021Review
- Immunotherapy using IgE or CAR T cells for cancers expressing the tumor antigen SLC3A2.Journal for immunotherapy of cancer · 2021Article
- Heteromeric Solute Carriers: Function, Structure, Pathology and Pharmacology.Advances in experimental medicine and biology · 2021Review
- Identification of AR-V7 downstream genes commonly targeted by AR/AR-V7 and specifically targeted by AR-V7 in castration resistant prostate cancer.Translational oncology · 2021Article
- MARCH Proteins Mediate Responses to Antitumor Antibodies.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Regulation of stem cell function and neuronal differentiation by HERV-K via mTOR pathway.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
CD98hc (SLC3A2) is the heavy chain component of the dimeric transmembrane glycoprotein CD98, which comprises the large neutral amino acid transporter LAT1 (SLC7A5) in cells. Overexpression of CD98hc occurs widely in cancer cells and is associated with poor prognosis clinically, but its exact contributions to tumorigenesis are uncertain. In this study, we showed that genetic deficiency of CD98hc protects against Ras-driven skin carcinogenesis. Deleting CD98hc after tumor induction was also sufficient to cause regression of existing tumors. Investigations into the basis for these effects defined two new functions of CD98hc that contribute to epithelial cancer beyond an intrinsic effect of CD98hc on tumor cell proliferation. First, CD98hc increased the stiffness of the tumor microenvironment. Second, CD98hc amplified the capacity of cells to respond to matrix rigidity, an essential factor in tumor development. Mechanistically, CD98hc mediated this stiffness sensing by increasing Rho kinase (ROCK) activity, resulting in increased transcription mediated by YAP/TAZ, a nuclear relay for mechanical signals. Our results suggest that CD98hc contributes to carcinogenesis by amplifying a positive feedback loop, which increases both extracellular matrix stiffness and resulting cellular responses. This work supports a rationale to explore the use of CD98hc inhibitors as cancer therapeutics.
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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.