Expression of Basic Fibroblast Growth Factor Correlates with Resistance to Paclitaxel in Human Patient Tumors

Gan, Yuebo; Wientjes, M. Guillaume; Au, Jessie L.-S.

doi:10.1007/s11095-006-0136-6

Cited by 70 publications

(64 citation statements)

References 42 publications

(22 reference statements)

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“…They also reported that treatment with an FGF2 antibody could inhibit FGF2-dependent proliferation and angiogenesis. Furthermore, Gan and colleagues reported that high FGF2 tumor levels reduced drug sensitivity, in part, due to the direct effects of FGF2 on proliferation and apoptosis (40). FGF2 activates the PI3K in endothelial cells (41), which regulate Akt or protein kinase B (PKB) activity (42).…”

Section: Discussionmentioning

confidence: 99%

Akt-Activated Endothelium Constitutes the Niche for Residual Disease and Resistance to Bevacizumab in Ovarian Cancer

Guerrouahen

Pasquier

Kaoud

et al. 2014

Molecular Cancer Therapeutics

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Section: Discussionmentioning

confidence: 99%

Akt-Activated Endothelium Constitutes the Niche for Residual Disease and Resistance to Bevacizumab in Ovarian Cancer

Guerrouahen

Pasquier

Kaoud

et al. 2014

Molecular Cancer Therapeutics

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“…31 Although these factors increase BCSC selfrenewal, they may also activate survival pathways which can artificially increase drug resistance. 41,42 Nanofiber scaffolds may offer an alternative to mammosphere culture as a way to propagate BCSC in vitro. The composition of these fibers can be controlled or modified to either inhibit or promote cellular differentiation.…”

mentioning

confidence: 99%

Enrichment of breast cancer stem-like cells by growth on electrospun polycaprolactone-chitosan nanofiber scaffolds

Sims‐Mourtada¹,

Niamat²,

Samuel³

et al. 2014

IJN

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A small population of highly tumorigenic breast cancer cells has recently been identified. These cells, known as breast-cancer stem-like cells (BCSC), express markers similar to mammary stem cells, and are highly resistant to chemotherapy. Currently, study of BCSC is hampered by the inability to propagate these cells in tissue culture without inducing differentiation. Recently, it was reported that proliferation and differentiation can be modified by culturing cells on electrospun nanofibers. Here, we sought to characterize the chemoresistance and stem-like properties of breast cancer cell lines grown on nanofiber scaffolds. Cells cultured on three-dimensional templates of electrospun poly( ε -caprolactone)-chitosan nanofibers showed increases in mammary stem cell markers and in sphere-forming ability compared with cells cultured on polystyrene culture dishes. There was no increase in proliferation of stem cell populations, indicating that culture on nanofibers may inhibit differentiation of BCSC. The increase in stemness was accompanied by increases in resistance to docetaxel and doxorubicin. These data indicate that BCSC populations are enriched in cells cultured on electrospun poly( ε -caprolactone)-chitosan nanofibers, scaffolds that may provide a useful system to study BCSC and their response to anticancer drug treatment.

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“…Some previous studies have shown that bFGF prevents chemotherapy induced apoptosis, which result in chemoresistance in many cancers such as small cell lung cancer and breast cancer. This antiapoptotic effect is mediated by MAPK/ERKs, PI3K/AKT and/ or PKC that increase the expression and activation of several anti-apoptotic proteins including Bcl-2, Bcl-X L and XIAP (16,17). Although the precise mechanisms of drug resistance in melanoma cells are largely unknown, targeted inhibition of bFGF/FGFR-1 in primary and metastatic melanoma cells blocks tumor growth by inducing apoptosis indicating a critical pro-survival role of bFGF in melanoma (7).…”

Section: Discussionmentioning

confidence: 99%

Monoclonal antibodies targeting basic fibroblast growth factor inhibit the growth of B16 melanoma in vivo and in vitro

Wang²,

Jin³

et al. 2010

Oncol Rep

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Abstract. Up-regulated basic fibroblast growth factor (bFGF or FGF-2) plays an important role in the development and metastasis of melanoma; therefore, neutralizing antibodies to bFGF may suppress melanoma growth. In this study, we have developed three monoclonal antibodies against bFGF (anti-bFGF mAbs), which display remarkable anti-tumor and anti-angiogenic effects in vitro and in vivo. Anti-bFGF mAbs significantly inhibit the proliferation and induce apoptosis of B16 cells, and show inhibitory effects on the migration of B16F10 cells and the tube formation of human umbilical vein endothelial cells (HUVECs) in vitro. Treatment of B16 melanoma spheroids with anti-bFGF mAbs in vivo results in significant reduction in tumor size and prolonged survival time of animals. Moreover, TUNEL (terminal transferase dUTP nick end labeling) assay and CD31 staining confirmed the increase of apoptosis and decrease of intratumoral microvessel density in tumor sections from animals treated with anti-bFGF mAbs. Our data indicate that anti-bFGF mAbs are potential therapeutic candidates for melanoma therapy by effectively suppressing the melanoma growth through inhibition of angiogenesis and induction of apoptosis in the tumor. IntroductionMelanoma is the most lethal form of skin cancer; it is usually resistant to both chemotherapy and radiotherapy. Therefore, biological approaches such as antibody targeted therapy and immunotherapy (cytokine and vaccine) have been recently focused on for the treatment of melanoma (1). bFGF belongs to the family of heparin-binding growth factors. Acting as a broad-spectrum mitogen and potent angiogenic agent, bFGF mediates a variety of cellular responses in embryonic development, wound healing or tumor growth (2). bFGF functions mainly by interacting with high affinity tyrosine kinase FGF receptors (FGFRs) on the surface of target cells. Upon binding to bFGF, FGFRs dimerize and are tyrosine phosphorylated, leading to the activation of downstream signaling pathways including MAPKs (mitogenactivated protein kinases)/ERKs (extracellular signal-regulated kinases) and PI3K (phosphoinositide 3-kinase)/AKT (protein kinase B) (3).The expression of bFGF is absent in normal melanocytes, which require exogenous bFGF to maintain the growth. bFGF transduced normal melanocytes exhibit transformed phenotype resembling early-stage melanoma, indicating a critical role of bFGF in the transformation of melanocytes to melanoma (4,5). Most melanomas express high levels of bFGF and FGFRs, which form an autocrine loop and are critical for the survival and growth of melanoma cells; melanoma growth can be arrested by interfering with the production or biological activity of bFGF alone (6,7). bFGF has long been regarded as an important tumor angiogenic factor and the specific roles of bFGF in angiogenesis and spontaneous metastasis of melanoma have also been revealed (8,9). These reports suggest the potential of bFGF as a target for melanoma therapy. Antisense targeting of bFGF/FGFR-1 in primary and metastatic melanoma cell...

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Expression of Basic Fibroblast Growth Factor Correlates with Resistance to Paclitaxel in Human Patient Tumors

Abstract: These results support a role of bFGF in paclitaxel resistance in human patient tumors.

Cited by 70 publications

References 42 publications

Akt-Activated Endothelium Constitutes the Niche for Residual Disease and Resistance to Bevacizumab in Ovarian Cancer

Akt-Activated Endothelium Constitutes the Niche for Residual Disease and Resistance to Bevacizumab in Ovarian Cancer

Enrichment of breast cancer stem-like cells by growth on electrospun polycaprolactone-chitosan nanofiber scaffolds

Monoclonal antibodies targeting basic fibroblast growth factor inhibit the growth of B16 melanoma in vivo and in vitro

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