ArticleScientific reports2018
Increase in resistance to anticancer drugs involves occludin in spheroid culture model of lung adenocarcinoma A549 cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 19 citations in OpenAlex.
- Photocrosslinkable lung dECM hydrogels promote stiffness-dependent lung cancer growth and chemoresistance.Materials today. Bio · 2026Article
- Selenium Nanoparticles Synergize with a KRAS Nanovaccine against Breast Cancer.Advanced healthcare materials · 2025Article
- Occludin: a gatekeeper of brain Infection by HIV-1.Fluids and barriers of the CNS · 2023Review
- p‑STAT3 influences doxorubicin and etoposide resistance of A549 cells grown in anOncology reports · 2023Article
- Real-Time Fluorescence Visualization and Quantitation of Cell Growth and Death in Response to Treatment in 3D Collagen-Based Tumor Model.International journal of molecular sciences · 2022Article
- Synthesis, Biological Activity, and Molecular Modelling Studies of Naphthoquinone Derivatives as Promising Anticancer Candidates Targeting COX-2.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Key genes and drug delivery systems to improve the efficiency of chemotherapy.Cancer drug resistance (Alhambra, Calif.) · 2021Article
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8 authors at 3 institutions in 1 country.
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Abstract
Chemoresistance is a serious issue in the therapy of many cancers, but the molecular mechanism is little understood. The mRNA level of occludin (OCLN), a tight junctional protein, was increased in the cisplatin (CDDP), doxorubicin (DXR), 7-ethyl-10-hydroxy-camptothecin, or gemcitabine-resistant human lung adenocarcinoma A549 cells. Here, we investigated the regulatory mechanism and pathophysiological role of OCLN. OCLN was mainly localized at tight junctions in A549 and CDDP-resistant A549 (A549/CDDP) cells. The level of p-Akt in A549/CDDP cells was higher than that in A549 cells, and the mRNA and protein levels of OCLN were suppressed by a phosphoinositide 3-kinase (PI3K)/Akt pathway inhibitor, LY-294002, suggesting that a PI3K/Akt pathway is involved in the elevation of OCLN expression. The overexpression of OCLN in A549 cells decreased paracellular permeability to DXR. Cytotoxicity to CDDP was unaffected by OCLN-overexpression in 2D culture model. In 3D culture model, the spheroid size, hypoxic level, and cell viability were significantly elevated by CDDP resistance, but not by OCLN-overexpression. The accumulation inside the spheroids and toxicity of DXR were correlated with OCLN expression. Our data suggest that OCLN is not directly involved in the chemoresistance, but it enhances chemoresistance mediated by suppression of accumulation of anticancer drugs inside the spheroids.
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