Follicle-Stimulating Hormone Peptide Can Facilitate Paclitaxel Nanoparticles to Target Ovarian Carcinoma <i>In vivo</i>

Zhang, Xiaoyan; Chen, Jun; Zheng, Yufang; Gao, Xiaoling; Kang, Yu; Liu, Jia-chi; Cheng, Mingjun; Sun, Hong; Xu, Congjian

doi:10.1158/0008-5472.can-08-4721

Cited by 88 publications

(86 citation statements)

References 44 publications

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“…Gonadotropins activate the MAPK/ERK1/2 signalling pathway in EOC cells OVCAR-3 cells have previously been shown to express the FSHR (Choi et al 2002, Zhang et al 2009). To confirm the expression of both FSHR and LHR, OV207 and OVCAR-3 cells were subjected to immunofluorescent staining (Supplementary Figure 1A and B, see section on supplementary data given at the end of this article), which clearly indicated the presence of both receptors in both cell types.…”

Section: Resultsmentioning

confidence: 99%

Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase Cδ

Mertens‐Walker¹,

Bolitho²,

Baxter³

et al. 2010

Endocrine-Related Cancer

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The gonadotropin hypothesis proposes that elevated serum gonadotropin levels may increase the risk of epithelial ovarian cancer (EOC). We have studied the effect of treating EOC cell lines (OV207 and OVCAR-3) with FSH or LH. Both gonadotropins activated the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) pathway and increased cell migration that was inhibited by the MAPK 1 inhibitor PD98059. Both extra-and intracellular calcium ion signalling were implicated in gonadotropin-induced ERK1/2 activation as treatment with either the calcium chelator EGTA or an inhibitor of intracellular calcium release, dantrolene, inhibited gonadotropin-induced ERK1/2 activation. Verapamil was also inhibitory, indicating that gonadotropins activate calcium influx via L-type voltage-dependent calcium channels. The cAMP/protein kinase A (PKA) pathway was not involved in the mediation of gonadotropin action in these cells as gonadotropins did not increase intracellular cAMP formation and inhibition of PKA did not affect gonadotropin-induced phosphorylation of ERK1/2. Activation of ERK1/2 was inhibited by the protein kinase C (PKC) inhibitor GF 109203X as well as by the PKCd inhibitor rottlerin, and downregulation of PKCd was inhibited by small interfering RNA (siRNA), highlighting the importance of PKCd in the gonadotropin signalling cascade. Furthermore, in addition to inhibition by PD98059, gonadotropin-induced ovarian cancer cell migration was also inhibited by verapamil, GF 109203X and rottlerin. Similarly, gonadotropin-induced proliferation was inhibited by PD98059, verapamil, GF 109203X and PKCd siRNA. Taken together, these results demonstrate that gonadotropins induce both ovarian cancer cell migration and proliferation by activation of ERK1/2 signalling in a calcium-and PKCd-dependent manner.

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Section: Resultsmentioning

confidence: 99%

Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase Cδ

Mertens‐Walker¹,

Bolitho²,

Baxter³

et al. 2010

Endocrine-Related Cancer

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“…FSH affects various aspects of ovarian cancer metastasis, such as it suppresses apoptosis, supports tumor growth by inducing increased expression of VEGFA (VEGF), facilitates blood vessel growth, and may alter certain oncogenic pathways that facilitate proliferative and invasive phenotype. Indeed, studies using nanoparticles conjugated to the b subunit of FSH showed a lot of promise both in vitro and in vivo to increase the specificity and delivery of chemotherapeutic drugs (Zhang et al 2009). …”

Section: Introductionmentioning

confidence: 99%

FSH–FSHR3–stem cells in ovary surface epithelium: basis for adult ovarian biology, failure, aging, and cancer

Bhartiya

Singh

2015

Reproduction

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Despite extensive research, genetic basis of premature ovarian failure (POF) and ovarian cancer still remains elusive. It is indeed paradoxical that scientists searched for mutations in FSH receptor (FSHR) expressed on granulosa cells, whereas more than 90% of cancers arise in ovary surface epithelium (OSE). Two distinct populations of stem cells including very small embryonic-like stem cells (VSELs) and ovarian stem cells (OSCs) exist in OSE, are responsible for neo-oogenesis and primordial follicle assembly in adult life, and are modulated by FSH via its alternatively spliced receptor variant FSHR3 (growth factor type 1 receptor acting via calcium signaling and the ERK/MAPK pathway). Any defect in FSH-FSHR3-stem cell interaction in OSE may affect folliculogenesis and thus result in POF. Ovarian aging is associated with a compromised microenvironment that does not support stem cell differentiation into oocytes and further folliculogenesis. FSH exerts a mitogenic effect on OSE and elevated FSH levels associated with advanced age may provide a continuous trigger for stem cells to proliferate resulting in cancer, thus supporting gonadotropin theory for ovarian cancer. Present review is an attempt to put adult ovarian biology, POF, aging, and cancer in the perspective of FSH-FSHR3-stem cell network that functions in OSE. This hypothesis is further supported by the recent understanding that: i) cancer is a stem cell disease and OSE is the niche for ovarian cancer stem cells; ii) ovarian OCT4-positive stem cells are regulated by FSH; and iii) OCT4 along with LIN28 and BMP4 are highly expressed in ovarian cancers.Reproduction (2015) 149 R35-R48

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“…Subsequently, 1 mL of each of the reconstituted PTX-SNs and PTX-HSNs (3 mg/mL) was added to the dialysis tubing attached to a support, and the release of PTX was determined according to Apparatus 2 of the Unites States Pharmacopeia (USP) dissolution method (paddle method). The release test was performed with 900 mL of the release medium at 100 rpm and 37°C; 1 mL of the released sample was collected at each time point (1,3,6,12,24,36,48,72,96,120, and 144 h). The content of PTX in each sample was measured using the HPLC method described.…”

mentioning

confidence: 99%

Paclitaxel-loaded hyaluronan solid nanoemulsions for enhanced treatment efficacy in ovarian cancer

Kim¹,

Park²

2017

IJN

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Follicle-Stimulating Hormone Peptide Can Facilitate Paclitaxel Nanoparticles to Target Ovarian Carcinoma In vivo

Cited by 88 publications

References 44 publications

Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase Cδ

Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase Cδ

FSH–FSHR3–stem cells in ovary surface epithelium: basis for adult ovarian biology, failure, aging, and cancer

Paclitaxel-loaded hyaluronan solid nanoemulsions for enhanced treatment efficacy in ovarian cancer

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