ArticleWorld journal of surgical oncology2014
Secreted clusterin (sCLU) regulates cell proliferation and chemosensitivity to cisplatin by modulating ERK1/2 signals in human osteosarcoma cells.
Article in World journal of surgical oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Unlocking the potential of marine natural product fragments for rational anticancer drug design: a computational approach.Scientific reports · 2026Article
- Clusterin Deficiency Promotes Cellular Senescence in Human Astrocytes.Molecular neurobiology · 2025Article
- Clusterin facilitates glioma progression via BCL2L1-dependent regulation of apoptotic resistance.Frontiers in molecular neuroscience · 2025Article
- Review
- The therapeutic and prognostic role of clusterin in diverse musculoskeletal diseases: a mini review.Physiological research · 2022Review
- Transcriptomic analysis reveals dynamic molecular changes in skin induced by mechanical forces secondary to tissue expansion.Scientific reports · 2020Article
- Clusterin role in hepatocellular carcinoma patients treated with oxaliplatin.Bioscience reports · 2020Article
- Hippo/YAP signaling pathway is involved in osteosarcoma chemoresistance.Chinese journal of cancer · 2016Article
- Characterization of site-specific glycosylation of secreted proteins associated with multi-drug resistance of gastric cancer.Oncotarget · 2016Article
- miRNA-378 reverses chemoresistance to cisplatin in lung adenocarcinoma cells by targeting secreted clusterin.Scientific reports · 2016Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral studies have shown that secreted clusterin (sCLU) up-regulation in multi-drug resistant osteosarcoma (OS) cells relates to enhanced drug resistance. Furthermore, sCLU silencing directed against sCLU induces significant reduction of cellular growth and sensitizes OS cells to chemotherapy. However, the molecular mechanisms underlying the effect of sCLU on OS cells are not known.
methodsTo evaluate the roles and possible mechanisms of sCLU in chemoresistance of OS cells to cisplatin (DPP), we utilized RNA interference to knockdown sCLU expression in the sCLU-rich U-2 OS cells and to overexpress sCLU in the sCLU-poorer KH OS cells, and further assessed the cell viability and chemosensitivity to DDP as well as possible signaling transduction pathways.
resultsThe data showed that sCLU depletion inhibited growth and sensitized sCLU-rich U-2 OS cells to cisplatin in vitro and in vivo by inducing inactivation of ERK1/2, and sCLU overexpression promoted growth and increased resistance of sCLU-less KH OS cells to cisplatin in vitro and in vivo by activation of ERK1/2.
conclusionsThe data also suggests critical roles of sCLU in OS cell chemoresistance to DPP and raises the possibility of sCLU depletion as a promising approach to OS therapy.
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