Alendronate inhibits cell invasion and MMP-2 secretion in human chondrosarcoma cell line

Lai, Te Jen; Hsu, Sheng Feng; Li, Te Mao; Hsu, Hsiang‐Chen; Lin, Jaung Geng; Chou, Ming Chih; Lee, Meng Chih; Yang, Shun Fa; Fong, Yi Chin

doi:10.1111/j.1745-7254.2007.00607.x

Cited by 25 publications

(19 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As showed previously by other studies [4,6,11], we observed MMP-2 activation and no effect of pamidronate in this result. Several studies showed inhibit MMP-2 activation when bisphosphonates were used [20][21][22]; however, Gonçalves et al [43] indicated that pamidronate did not affect MMP activation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pamidronate Attenuates Oxidative Stress and Energetic Metabolism Changes but Worsens Functional Outcomes in Acute Doxorubicin-Induced Cardiotoxicity in Rats

Carvalho

Gonçalves

Alegre

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Cardiotoxicity is the major side effect of doxorubicin. As mechanisms that are involved in cardiotoxicity are ambiguous, new methods for attenuating cardiotoxicity are needed. Recent studies have shown that bisphosphonates can decrease oxidative stress. Therefore, the objective of this study was to evaluate the effect of pamidronate on preventing acute doxorubicin-induced cardiotoxicity. Methods: Sixty-four male Wistar rats were allocated into four groups: the control group (C), the pamidronate group (P), the doxorubicin group (D) and the doxorubicin/pamidronate group (DP). The rats in the P and DP groups received pamidronate injections (3 mg/kg, IP). After 24 hours, the rats in the D and DP groups received doxorubicin injections (20 mg/kg, IP). Forty-eight hours after doxorubicin injection, the rats were killed. Echocardiography, isolated heart study and biochemical analysis were performed. Results: Doxorubicin-induced acute cardiotoxicity showed increased matrix metalloproteinases (MMP)-2 activation, oxidative damage and induced alterations in myocardial energetic metabolism. Pamidronate did not inhibit MMP-2 activation but attenuated oxidative stress and improved myocardial energetic metabolism. Regarding cardiac function, the DP group exhibited a decrease in the left ventricular ejection fraction in the echocardiography and a decrease in +dP/dt in the isolated heart study compared with other groups. The same DP group presented serum hypocalcaemia. Conclusions: Despite its ability to reduce oxidative stress and improve energy metabolism in the heart, pamidronate worsened systolic function in rats treated with doxorubicin, and therefore we cannot recommend its use in conjunction with anthracycline chemotherapy.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The recent use of bisphosphonates was associated with decreased MMP activation [20][21][22]. In addition, bisphosphonates treatment in patients with several types of cancer decreased serum lipid hydroperoxide levels and increased serum glutathione peroxidase levels [23].…”

Section: Introductionmentioning

confidence: 99%

Pamidronate Attenuates Oxidative Stress and Energetic Metabolism Changes but Worsens Functional Outcomes in Acute Doxorubicin-Induced Cardiotoxicity in Rats

Carvalho

Gonçalves

Alegre

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Because N-BPs have been shown to exert anti-tumour effects in vitro, recent works have been performed on chondrosarcoma cell lines. Thus, Lai et al demonstrated that alendronate inhibits JJ012 chondrosarcoma cell invasion and MMP-2 expression/activity in a dosedependent manner [88]. These data have been confirmed by Susa et al in 2009 who showed that alendronate decreased the viability of human CS-1 chondrosarcoma cell line by inhibiting simultaneously proliferation and migration [89].…”

Section: Bisphosphonates and Treatment Of Chondro-sarcomasmentioning

confidence: 73%

Therapeutic Approach of Primary Bone Tumours by Bisphosphonates

Moriceau¹,

Ory²,

Gobin³

et al. 2010

CPD

View full text Add to dashboard Cite

Bone tumours can be dissociated in two main categories: i) primary bone tumours (benign or malignant) including mainly osteosarcoma and other sarcomas.ii)and giant cell tumour and bone metastases originate from others cancer (Breast, prostate, kidney cancer, etc). These tumours are able to destroy or/and induce a new calcified matrix. However, the first step of bone tumour development is associated with an induction of bone resorption and the establishment of a vicious cycle between the osteoclasts and the tumour growth. Indeed, bone resorption contributes to the pathogenesis of bone tumour by the release of cytokines (IL6, TNFα) which govern the bone tumour's development and which are trapped into the bone matrix. Bisphosphonates (BPs) are chemical compounds of P-C-P structure with a high affinity for bone hydroxyapatite crystals. Thus, they have been used as a carrier for radio nucleotides to develop novel approaches of bone imaging. BPs exert also indirect anti-tumour activities in vivo. Indeed, BPs directly interfere with the bone microenvironment and target osteoclasts, endothelial cells and immune cells (tumour-associated macrophages, γ9δ2 T cells). BPs induce tumour cell death in vitro and same activity is suspected in vivo. The present review summarizes the mechanisms of actions of BPs as well as their clinical interests in bone primary tumours.

show abstract

“…4D). Aln has been shown to reduce the activity and mRNA levels of MMP-2 and inhibit cell invasion in the chondrosarcoma cell line (39). APC can inhibit MMP-9 via NF-κB, while at the same time promoting MMP-2 activity (34).…”

Section: Apc Protects Endothelial Cells From Bisphosphonate-induced Dmentioning

confidence: 99%

Activated protein C inhibits bisphosphonate-induced endothelial cell death via the endothelial protein C receptor and nuclear factor-κB pathways

Park

2011

Int J Mol Med

View full text Add to dashboard Cite

Abstract.Bisphosphonates promote apoptosis of cancer cells as well as osteoclasts in bone metastatic sites, but several clinical trials and high concentration treatment have shown that bisphosphonates have side effects that include bone loss and damage to normal cells. The aim of this study was to elucidate the protective effect and the possible mechanism of activated protein C (APC) against bisphosphonate-induced cell damage using primary cultured human umbilical vein endothelial cells (HUVECs). HUVECs were treated with APC (10 μg/ml) for 1 h, and then treated with bisphosphonates including alendronate, zoledronate and pamidronate. Bisphosphonates induced cell death in HUVECs but the cell death was blocked by treatment with APC. Bisphosphonates markedly induced caspase-3 activation, which was diminished in cells exposed to APC. Matrix metalloproteinase-2 (MMP-2) reduction and nuclear factor-κB (NF-κB) activation induced by bisphosphonates in HUVECs were also blocked by APC treatment. Furthermore, APC highly induced the expression of the endothelial protein c receptor (EPCR) in HUVEC cells. In conclusion, the present study demonstrates that APC inhibits bisphosphonate-induced endothelial cell death via EPCR-induced inactivation of caspase-3 and NF-κB, and also suggests that APC has the potential to be a therapeutic drug in various vascular diseases induced by endothelial cell damage.

show abstract

Alendronate inhibits cell invasion and MMP-2 secretion in human chondrosarcoma cell line

Cited by 25 publications

References 29 publications

Pamidronate Attenuates Oxidative Stress and Energetic Metabolism Changes but Worsens Functional Outcomes in Acute Doxorubicin-Induced Cardiotoxicity in Rats

Pamidronate Attenuates Oxidative Stress and Energetic Metabolism Changes but Worsens Functional Outcomes in Acute Doxorubicin-Induced Cardiotoxicity in Rats

Therapeutic Approach of Primary Bone Tumours by Bisphosphonates

Activated protein C inhibits bisphosphonate-induced endothelial cell death via the endothelial protein C receptor and nuclear factor-κB pathways

Contact Info

Product

Resources

About