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- W2322313656 abstract "Tumor cell-derived hyaluronidase HYAL1, which degrades hyaluronic acid (HA), promotes tumor growth and metastasis. In prostate cancer (CaP), HYAL1 expression in biopsy and prostatectomy specimens is an independent prognostic marker for predicting disease progression. Sulfated hyaluronic acid (sHA) inhibits HYAL1 activity through a mixed inhibition mechanism. Antitumor activity of sHA has not been evaluated. In this study we evaluated effects of sHA on CaP cells. The effect of sHA (0-40 ug/ml) on cell proliferation and apoptosis was examined in CaP cells (PC3-ML, LNCaP, LNAI, C4-2B, LAPC-4, DU145, RWPE1) by cell counting and Cell Death ELISA kit. Matrigel invasion and Boyden chamber assays were used to test the effect of sHA on invasive activity. Effect of sHA on signaling, apoptosis cascade, androgen receptor activity, VEGF, NFkB activity, and HA receptor levels, was evaluated by immunoblotting, Q-PCR and reporter assays. Athymic mice bearing LNAI xenografts were treated with sHA (25 and 50 mg/kg) by i.p. injection. sHA inhibited proliferation, motility and invasion in CaP cells. At IC 50 for HAase activity inhibition (∼ 10-μg/ml), sHA induced > 3-fold apoptosis and inhibited invasive activity of CaP cells, which could be partially reversed by HA-fragments. sHA induced caspase-3, -8, -9 activation, up-regulation of Fas, Fas-L, FADD, and DR4 and down regulated bcl-2, phospho-bad, bcl-XL, phospho-Akt, phospho-IkB, and phospho-AR. At IC 50 , sHA caused > 90% inhibition of NFKB-reporter activity, PSA-promoter activity and transcriptionally down regulated HA-receptors (CD44 and RHAMM) and VEGF. Effect of sHA could be reversed by overexpression of m-Akt. Down regulation of CD44 and RHAMM, together with sHA synergistically inhibited cell proliferation and Akt activation. sHA significantly inhibited LNAI tumor growth. The majority of the animals did not form palpable tumors at 50-mg/kg dose even after 70 days when the treatment was stopped on 42 nd day. No weight loss or serum and organ toxicity was observed in sHA treated animals. Tumors showed reduced microvessel density (∼3-fold) and increased TUNEL positive cells (> 5-fold). This is the first study that shows targeting HYAL1 (by sHA – a novel non-toxic agent), may control CaP growth and progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2589. doi:10.1158/1538-7445.AM2011-2589" @default.
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- W2322313656 date "2011-04-15" @default.
- W2322313656 modified "2023-09-27" @default.
- W2322313656 title "Abstract 2589: Sulfated hyaluronic acid: A possible targeted therapy for prostate cancer" @default.
- W2322313656 doi "https://doi.org/10.1158/1538-7445.am2011-2589" @default.
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