Effect of the combination of a cyclooxygenase-1 selective inhibitor and taxol on proliferation, apoptosis and angiogenesis of ovarian cancer in vivo

Li, Wei; Liu, Meilin; Cai, Jiahui; Tang, Yun-Xian; Zhai, Ling; Zhang, Jun

doi:10.3892/ol.2012.688

Cited by 16 publications

(15 citation statements)

References 40 publications

(49 reference statements)

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“…Li found similar results in their in vivo studies (Li et al, 2012a). Li and colleagues also investigated the combination of SC-560 and taxol as well as celecoxib and taxol on the effect of SKOV-3 tumor MVD, apoptosis and VEGF transcript levels (Li et al, 2012a). Taxol in combination with SC-560 was superior to taxol with celecoxib and while the authors did not provide an explanation for the observed differences in the two inhibitors, the potential remains for the possibility of off target or non-COX related effects of the inhibitors (Li et al, 2012a;Li et al, 2013).…”

Section: Cox Enzymes In Ovarian Cancersupporting

confidence: 75%

The Role of Eicosanoids in Gynecological Malignancies

et al. 2020

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Eicosanoids, bio-active lipid molecules, evoke a multitude of biological effects that directly affect cancer cells and indirectly affect tumor microenvironment. An emerging role has been shown for eicosanoids in the pathogenesis of gynecological malignancies which include cancers of the vulva, vagina, cervix, uterine, and ovary. Eicosanoid biosynthesis pathways start at the metabolism of phospholipids by phospholipase A2 then proceeding to one of three pathways: the cyclooxygenase (COX), lipoxygenase (LOX), or P450 epoxygenase pathways. The most studied eicosanoid pathways include COX and LOX; however, more evidence is appearing to support further study of the P450 epoxygenase pathway in gynecologic cancers. In this review, we present the current knowledge of the role of COX, LOX and P450 pathways in the pathogenesis of gynecologic malignancies. Vulvar and vaginal cancer, the rarest subtypes, there is association of COX-2 expression with poor disease specific survival in vulvar cancer and, in vaginal cancer, COX-2 expression has been found to play a role in mucosal inflammation leading to disease susceptibility and transmission. Cervical cancer is associated with COX-2 levels 7.4 times higher than in healthy tissues. Additionally, HPV elevates COX-2 levels through the EGFR pathway and HIV promotes elevated COX-2 levels in cervical tissue as well as increases PGE 2 levels eliciting inflammation and progression of cancer. Evidence supports significant roles for both the LOX and COX pathways in uterine cancer. In endometrial cancer, there is increased expression of 5-LOX which is associated with adverse outcomes. Prostanoids in the COX pathway PGE 2 and PGF 2α have been shown to play a significant role in uterine cancer including alteration of proliferation, adhesion, migration, invasion, angiogenesis, and the inflammatory microenvironment. The most studied gynecological malignancy in regard to the potential role of eicosanoids in tumorigenesis is ovarian cancer in which all three pathways have shown to be associated or play a role in ovarian tumorigenesis directly on the tumor cell or through modulation of the tumor microenvironment. By identifying the gaps in knowledge, additional pathways and targets could be identified in order to obtain a better understanding of eicosanoid signaling in gynecological malignancies and identify potential new therapeutic approaches.

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Section: Cox Enzymes In Ovarian Cancersupporting

confidence: 75%

The Role of Eicosanoids in Gynecological Malignancies

et al. 2020

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“…The balance between the proangiogenic and antiangiogenic molecules released by tumor cells and surrounding host cells determines the intense tumor vascularization. Previous studies have demonstrated that VEGF-positive tissue was associated with a high MVD expression, whereas VEGF-negative tissue demonstrated a low expression of MVD, suggesting a positive correlation between VEGF and MVD (28). This result suggests that the potent antiangiogenic activity of brivanib is the primary mechanism of the inhibition of tumor growth in a Hep3B xenograft animal model.…”

Section: Discussionsupporting

confidence: 60%

Characterization of brivanib therapy response in hepatocellular carcinoma xenografts using 1H HR-MAS spectroscopy and histopathology

Yang

Song

Kim

et al. 2013

Molecular Medicine Reports

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Abstract. Angiogenesis inhibition is an attractive therapeutic strategy in the management of solid tumors. Vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF) are key factors in growth and neovascularization of hepatocellular carcinoma (HCC). Brivanib is a novel, orally available dual tyrosine kinase inhibitor that selectively targets the key angiogenesis receptors VEGF-R2, FGF-R1 and FGF-R2. Recently, high-resolution magic angle spinning magnetic resonance spectroscopy (HR-MAS MRS) has provided the opportunity to investigate more detailed metabolic profiles from intact tissue specimens that are correlated with histopathology and is thus, a promising tool for monitoring changes induced by treatment. In the present study, 1 H HR-MAS MRS and immunohistochemistry were used to investigate the antitumor efficacy of brivanib in HCC xenograft models. Tumor growth was significantly suppressed in brivanib-treated mice compared with the controls and treatment was associated with the inhibition of angiogenesis, increased apoptosis and inhibition of cell proliferation. Furthermore, HR-MAS techniques showed altered metabolic profiles between the two groups. HR-MAS spectra demonstrated a significant decrease in choline metabolite levels in the treated groups, concurrent with decreased cell proliferation and increased apoptosis. The results showed that 1 H HR-MAS MRS provides quantitative metabolite information that may be used to analyze the efficacy of brivanib treatment in Hep3B tumor xenografts. Thus, the HR-MAS MRS technique may be a complementary method to support histopathological results and increase its potential for use in the clinic.

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“…Celecoxib and diclofenac involved VEGF signaling, 45,52) whereas SC-560 did not. 53) Therefore, from the point of view of a decrease in the prevalence of adverse events such as HT and HFSR, SC-560 is recommended in combination with sorafenib for the treatment of HCC. Furthermore, the QOL was considered to be improved in these patients.…”

Section: )mentioning

confidence: 99%