ArticleOncogene2017
Serglycin in tumor microenvironment promotes non-small cell lung cancer aggressiveness in a CD44-dependent manner.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 129 citations in OpenAlex.
- Intermittent fasting from dawn to sunset for four consecutive weeks induces anticancer serum proteome response and improves metabolic syndrome.Scientific reports · 2020Trial
- Spatial and single-cell transcriptomic profiling reveals interplay between SRGN-associated epithelial programs and C1QC+ macrophages in early LUAD progression.Journal of translational medicine · 2026Article
- Article
- Hypoxia-induced secretory autophagy in cancer-associated fibroblasts promotes ECM remodelling through serglycin secretion in oral squamous cell carcinoma.Clinical and translational medicine · 2025Article
- Identification of anoikis-related tumor microenvironment characteristics and prognostic signature in ovarian cancer at bulk and single-cell levels.Discover oncology · 2025Article
- Exploring the Role of CDO1 in Breast Cancer: Insights into Tumor Biology and Therapeutic Potential.Annals of surgical oncology · 2025Article
- Anoikis resistance in Cancer: Mechanisms, therapeutic strategies, potential targets, and models for enhanced understanding.Cancer letters · 2025Review
- The role of the tumour microenvironment in lung cancer and its therapeutic implications.Medical oncology (Northwood, London, England) · 2025Review
- Multi-Omics Analysis of the Epigenetic Effects of Inflammation in Murine Type II Pneumocytes.International journal of molecular sciences · 2025Article
- Cross-Regional Transcriptome Data Reveal Transcriptional Abnormalities Associated with Lung Adenocarcinoma.Reports of biochemistry & molecular biology · 2025Article
- SRGN-mediated reactivation of the YAP/CRISPLD2 axis promotes aggressiveness of hepatocellular carcinoma.International journal of biological sciences · 2025Article
- The role of transcription factors in the crosstalk between cancer-associated fibroblasts and tumor cells.Journal of advanced research · 2025Review
- The axis of tumor-associated macrophages, extracellular matrix proteins, and cancer-associated fibroblasts in oncogenesis.Cancer cell international · 2024Review
- SRGN amplifies microglia-mediated neuroinflammation and exacerbates ischemic brain injury.Journal of neuroinflammation · 2024Article
- Serglycin secreted by late-stage nucleus pulposus cells is a biomarker of intervertebral disc degeneration.Nature communications · 2024Article
- M6PR- and EphB4-Rich Exosomes Secreted by Serglycin-Overexpressing Esophageal Cancer Cells Promote Cancer Progression.International journal of biological sciences · 2023Article
- Cancer-associated fibroblasts: The chief architect in the tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Review
- Review
- Cancer-associated fibroblasts in nonsmall cell lung cancer: From molecular mechanisms to clinical implications.International journal of cancer · 2022Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor microenvironment (TME) plays an active role in promoting tumor progression. To further understand the communication between TME and tumor cells, this study aimed at investigating the involvement of CD44, a type I cell surface receptor, in the crosstalk between tumor cells and TME. We have previously shown that chondroitin sulfate proteoglycan serglycin (SRGN), a CD44-interacting factor, was preferentially secreted by cancer-associated fibroblasts (CAFs) for promoting tumor growth in breast cancer patients. In this study, we show that SRGN is overexpressed in primary non-small cell lung cancers (NSCLCs), by both carcinoma and stromal cells. Using gain-of-function and loss-of-function approaches, we show that SRGN promotes NSCLC cell migration and invasion as well as colonization in the lung and liver in a CD44-dependent manner. SRGN induces lung cancer cell stemness, as demonstrated by its ability to enhance NSCLC cell sphere formation via Nanog induction, accompanied with increased chemoresistance and anoikis-resistance. SRGN promotes epithelial-mesenchymal transition by enhancing vimentin expression via CD44/NF-κB/claudin-1 (CLDN1) axis. In support, CLDN1 and SRGN expression are tightly linked together in primary NSCLC. Most importantly, increased expression of SRGN and/or CLDN1 predicts poor prognosis in primary lung adenocarcinomas. In summary, we demonstrate that SRGN secreted by tumor cells and stromal components in the TME promotes malignant phenotypes through interacting with tumor cell receptor CD44, suggesting that a combined therapy targeting both CD44 and its ligands in the TME may be an attractive approach for cancer therapy.
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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.