Monitoring luciferase-labeled cancer cell growth and metastasis in different in vivo models

Nogawa, Masaki; Yuasa, Takeshi; Kimura, Shinya; Kuroda, Junya; Satô, Kiyoshi; Segawa, Hajime; Yokota, Asumi; Maekawa, Taira

doi:10.1016/j.canlet.2004.07.010

Cited by 71 publications

(55 citation statements)

References 17 publications

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“…Using this in vivo imaging system, we evaluated the efficacy of sunitinib by measuring the photon counts of the metastatic lesions in the mandible and both hip joints in a blinded manner as described previously. 13 …”

Section: Measurement Of Bone Metastatic Lesions By In Vivo Imagingmentioning

confidence: 99%

“…Of these mice, we excluded those that showed brilliant bioluminescence in the lungs. The remaining 14 mice were then divided into two matched groups according to bioluminescence quantified by IVIS, and we administered either sunitinib or vehicle control for 4 weeks and monitored the growth of bone metastases in the lesions in the maxilla and bilateral hip joints, as described previously 12,13 (Fig. 1b).…”

Section: Effect Of Sunitinib On Rcc Growth In a Mouse Bone Metastasismentioning

confidence: 99%

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Antitumor effect of sunitinib against skeletal metastatic renal cell carcinoma through inhibition of osteoclast function

Maita

Yuasa

Tsuchiya

et al. 2011

Intl Journal of Cancer

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We investigated the inhibitory effect of sunitinib, a newly approved multitargeted tyrosine kinase inhibitor, against the progression of renal cell cancer (RCC) bone metastases in vivo. In vitro cell proliferation was determined using the MTS assay. To investigate the inhibitory effects of sunitinib in vivo, we established luciferase-labeled ACHN Luc cells derived from papillary RCC. Mice in which ACHN Luc cells had been transplanted into the left ventricle to establish bone metastases were treated orally with 40 mg/kg/day sunitinib or vehicle control for 3 weeks. Growth of the cancer cells was monitored using an in vivo imaging system. In addition, 16 patients with metastatic RCC were treated with sunitinib, and serum and urine levels of amino-terminal telopeptide (NTx) were measured as markers of bone resorption. Sunitinib did not inhibit the growth of RCC cells in vitro at clinically or experimentally achievable serum levels (100 nM-1 lM). To investigate the inhibitory effect of sunitinib in vivo, we established luciferase-labeled human RCC cells (ACHN Luc ). Sunitinib prevented the growth of ACHN Luc RCC cells in the bone metastatic mouse model. The number of osteoclasts in sunitinib-treated mice was significantly less than that in control mice. Serum and urine levels of NTx in patients with metastatic RCC declined significantly during the first 4 weeks of sunitinib treatment (p 5 0.027). Sunitinib is a potent anticancer agent for RCC bone metastases, at least for papillary RCC.Bone is a common site of metastasis, with the frequency of solitary or multiple metastases to bone ranging from 24 to 51% in patients with metastatic renal cell cancer (RCC). 1-3 Although bone metastasis is not an independent prognostic factor associated with poor survival, the prognosis of patients with bone metastasis is not favorable when they are treated with cytokines, with an average life expectancy of 8-16 months. [2][3][4] Moreover, bone metastases are associated with poor performance status due to intractable pain and pathological fractures. 5 Because treatment options for RCC patients with bone metastasis are limited, appropriate treatment strategies are desired.Sunitinib is a newly approved, multitarget, small-molecule tyrosine kinase inhibitor for the treatment of metastatic RCC. It inhibits various receptor tyrosine kinases, including vascular endothelial growth factor (VEGF) receptors 1, 2 and 3; stem cell factor receptor (KIT) and PDGF receptors a and b. 6-8 Moreover, sunitinib has been known to inhibit the phosphorylation of colony-stimulating factor (CSF)-1R, resulting in the prevention of osteoclast function and CSF-1R-dependent osteolysis in an experimental breast cancer bone metastasis model. 9,10 These findings led us to propose the hypothesis that sunitinib may inhibit tumor growth and osteolysis in bone metastatic lesions in RCC patients.Although establishing a treatment strategy for bone metastases from RCC is important for urologists, the assessment of inhibitory effects on the growth of bone metastases is oft...

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Section: Measurement Of Bone Metastatic Lesions By In Vivo Imagingmentioning

confidence: 99%

Section: Effect Of Sunitinib On Rcc Growth In a Mouse Bone Metastasismentioning

confidence: 99%

Antitumor effect of sunitinib against skeletal metastatic renal cell carcinoma through inhibition of osteoclast function

Maita

Yuasa

Tsuchiya

et al. 2011

Intl Journal of Cancer

Self Cite

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“…Sixteen days later, the mice were killed, and the tumors were dissected. Tumor growth patterns were measured twice a week on the basis of the photons emitted from luciferaseexpressing cells counted using the light-light chamber of a CCD camera system (Xenogen, Alameda, CA, USA) (Nogawa et al, 2005). Approval for these studies was obtained from the Animal Research Committee of Graduate School of Medicine, Kyoto University.…”

Section: Immunoblotting and Immunoprecipitationmentioning

confidence: 99%

Cancer-specific enhancement of cisplatin-induced cytotoxicity with triptolide through an interaction of inactivated glycogen synthase kinase-3β with p53

et al. 2008

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To improve conventional chemotherapeutic efficacy, a combination use of traditional medicines is effective but detailed mechanisms have been rarely elucidated. In the this study, we attempted to clarify how triptolide (PG490), an oxygenated diterpene derived from a Chinese herb, enhances the cisplatin (CDDP)-induced cytotoxicity in urothelial cancer cells. Our results showed that a combined CDDP/triptolide therapy induced apoptosis in urothelial cancer cell lines with wild-type p53, but not in those with mutant-type p53 or normal human urothelium. As the mechanism, triptolide suppressed CDDP-induced p53 transcriptional activity, leading to p21 attenuation, which promoted apoptosis via the activation of c-Jun N-terminal kinase (JNK) and Bax. We further demonstrated that the functional regulation of p53 by triptolide was mediated by an intranuclear association of p53 with glycogen synthase kinase-3b (GSK3b), which was inactivated by protein kinase C (PKC). This modulation of the PKC-GSK3b axis by triptolide was observed in a cancer-specific manner. A mouse xenograft model also showed that a combined CDDP/triptolide therapy completely suppressed tumor growth without any side effects. We expect that cancer-specific enhancement of CDDP-induced cytotoxicity with triptolide may effectively overcome the resistance to a CDDP-based conventional chemotherapy as a treatment for urothelial cancer.

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“…Tumour growth was monitored using an in vivo imaging system (IVIS, Xenogen, Alameda, CA, USA) with an aqueous solution of luciferin (150 mg kg À1 intraperitoneally), as described previously (Nogawa et al, 2005a).…”

Section: Mouse Modelsmentioning

confidence: 99%

A third-generation bisphosphonate, minodronic acid (YM529), successfully prevented the growth of bladder cancer in vitro and in vivo

et al. 2006

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Minodronic acid (YM529) is a third-generation bisphosphonate (BP) that has been shown to directly and indirectly prevent proliferation, induce apoptosis, and inhibit metastasis of various types of cancer cells. In this study, we have investigated the therapeutic efficacy of YM529 against bladder cancer, both in vitro and in vivo. YM529 inhibited geranylgeranylation as well as farnesylation and reduced the growth of all seven bladder cancer cell lines in a dose-and time-dependent manner in vitro. YM529 demonstrated a good synergistic or additive antiproliferative effect when administered in combination with cisplatin or paclitaxel. Immunohistochemical study revealed YM529 inhibited the prenylation of Rap1A in vivo. YM529 administered systemically did not markedly inhibit the growth of visceral metastases but it showed a significant anticancer effect on bone metastases monitored by an in vivo imaging system. Moreover, intravesical YM529 demonstrated significant growth inhibition in a bladder cancer orthotopic model. No adverse effects were associated with the systemic as well as the intravesical treatment regimens. In conclusion, our study suggests that YM529 may be a potent anticancer agent for bladder cancer. The efficacy and safety of this BP as an agent for combination chemotherapies against bladder cancer should be verified by early-phase clinical trials.

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Monitoring luciferase-labeled cancer cell growth and metastasis in different in vivo models

Cited by 71 publications

References 17 publications

Antitumor effect of sunitinib against skeletal metastatic renal cell carcinoma through inhibition of osteoclast function

Antitumor effect of sunitinib against skeletal metastatic renal cell carcinoma through inhibition of osteoclast function

Cancer-specific enhancement of cisplatin-induced cytotoxicity with triptolide through an interaction of inactivated glycogen synthase kinase-3β with p53

A third-generation bisphosphonate, minodronic acid (YM529), successfully prevented the growth of bladder cancer in vitro and in vivo

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