ArticleCancer science2024
ARID1A loss induces P4HB to activate fibroblasts to support lung cancer cell growth, invasion, and chemoresistance.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 14 citations in OpenAlex.
- Development and validation of a nomogram based on three-dimensional quantitative parameters from dual-layer detector spectral computed tomography for predicting treatment response to neoadjuvant chemotherapy in pancreatic ductal adenocarcinoma.Journal of gastrointestinal oncology · 2026Article
- sc-rDSeq: a robust and cost-effective full-length total RNA sequencing method for single cells reveals multilayered heterogeneity in drug-resistant lung cancer cells.Nucleic acids research · 2026Article
- Multi-omics identification of a programmed cell death-related signature and potential target P4HB for bladder cancer based on a 101-combination machine learning and experimental validation.Clinical and experimental medicine · 2026Article
- Targeting collagen Prolyl 4-hydroxylase for cancer treatment.Medical oncology (Northwood, London, England) · 2025Review
- miR-188-5p accelerates intervertebral disc degeneration by mediating P4HB to regulate ferroptosis in nucleus pulposus cells.European journal of medical research · 2025Article
- Evaluation of induction chemotherapy response using multiphasic dual-energy CT in nasopharyngeal carcinoma.European radiology · 2025Article
- CHK1 inhibition increases the therapeutic response to radiotherapy via antitumor immunity in ARID1A-deficient colorectal cancer.Cell death & disease · 2025Article
- ARID1A silencing-mediated upregulation of microRNA-652 accelerates cigarette smoke-induced human bronchial epithelial cell transformation by targeting ZFAND5.BMC pulmonary medicine · 2025Article
- Nomogram based on dual-energy computed tomography to predict the response to induction chemotherapy in patients with nasopharyngeal carcinoma: a two-center study.Cancer imaging : the official publication of the International Cancer Imaging Society · 2025Article
- ARID1A deficiency attenuates the response to EGFR-TKI treatment in lung adenocarcinoma.Frontiers in pharmacology · 2025Article
- Article
- The Pivotal Role of Preclinical Animal Models in Anti-Cancer Drug Discovery and Personalized Cancer Therapy Strategies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Chromatin modifiers in human disease: from functional roles to regulatory mechanisms.Molecular biomedicine · 2024Review
- ARID1A loss induces P4HB to activate fibroblasts to support lung cancer cell growth, invasion, and chemoresistance.Cancer science · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Loss of AT-interacting domain-rich protein 1A (ARID1A) frequently occurs in human malignancies including lung cancer. The biological consequence of ARID1A mutation in lung cancer is not fully understood. This study was designed to determine the effect of ARID1A-depleted lung cancer cells on fibroblast activation. Conditioned media was collected from ARID1A-depleted lung cancer cells and employed to treat lung fibroblasts. The proliferation and migration of lung fibroblasts were investigated. The secretory genes were profiled in lung cancer cells upon ARID1A knockdown. Antibody-based neutralization was utilized to confirm their role in mediating the cross-talk between lung cancer cells and fibroblasts. NOD-SCID-IL2RgammaC-null (NSG) mice received tumor tissues from patients with ARID1A-mutated lung cancer to establish patient-derived xenograft (PDX) models. Notably, ARID1A-depleted lung cancer cells promoted the proliferation and migration of lung fibroblasts. Mechanistically, ARID1A depletion augmented the expression and secretion of prolyl 4-hydroxylase beta (P4HB) in lung cancer cells, which induced the activation of lung fibroblasts through the β-catenin signaling pathway. P4HB-activated lung fibroblasts promoted the proliferation, invasion, and chemoresistance in lung cancer cells. Neutralizing P4HB hampered the tumor growth and increased cisplatin cytotoxic efficacy in two PDX models. Serum P4HB levels were higher in ARID1A-mutated lung cancer patients than in healthy controls. Moreover, increased serum levels of P4HB were significantly associated with lung cancer metastasis. Together, our work indicates a pivotal role for P4HB in orchestrating the cross-talk between ARID1A-mutated cancer cells and cancer-associated fibroblasts during lung cancer progression. P4HB may represent a promising target for improving lung cancer treatment.
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