Mechanisms and Influence of Octreotide-Induced Regulation of Somatostatin Receptor 2 on Hepatocellular Carcinoma

Hua, Yunpeng; Yin, Xiaoyu; Peng, Baogang; Li, Shaoqiang; Lai, Jia-ming; Liang, Hui-zhen; Liu, Liang

doi:10.1159/000227763

Cited by 23 publications

(19 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results are also in agreement with data on hepatocellular carcinoma cell lines [26]. Our data are, however, not in agreement with the results obtained in prostate cancer cell lines by Erten et al [27], who reported that both docetaxel and octreotide decreased cell proliferation in a time-dependent and dose-dependent manner when using PC3wt and DU145 cells, indicating different roles of the two drugs on those cell lines.…”

Section: Discussionsupporting

confidence: 77%

Differential molecular mechanism of docetaxel–octreotide combined treatment according to the docetaxel-resistance status in PC3 prostate cancer cells

et al. 2013

View full text Add to dashboard Cite

To examine the effect and the molecular mechanisms of the combined treatment of the somatostatin (SST) analogue octreotide with docetaxel: analysis of proliferation, apoptosis and migration in the human prostate cancer cell line PC3, either sensitive (PC3wt) or made resistant to docetaxel (PC3R). We examined the effect of the two drugs individually or in combination on cell proliferation and migration by analysis of apoptosis and cell cycle proteins. The role of octreotide in modulating P-glycoprotein function was examined together with the modulation of SST receptors type 2 and 5 (SSTR2 and SSTR5). We observed an enhanced effect of docetaxel and octreotide given in combination or in sequence compared with either agent alone; this result was particularly evident when docetaxel was given before octreotide in PC3wt and when the two drugs were given together in PC3R cells. In contrast to lanreotide, our data indicate that octreotide does not act as a P-glycoprotein inhibitor in PC3R cells. A role of docetaxel and combined treatment in regulating SSTR2, SSTR5, proliferation and apoptosis gene expression is suggested as the possible mechanism for the enhanced effect observed. In addition, an evaluation of the effect of the combined treatment on cellular migration was examined, showing a moderate loss of invasive properties in PC3R cells. The present results confirm that SST analogues may be combined with docetaxel to increase the antitumour effect in patients with advanced prostate carcinoma.

show abstract

Section: Discussionsupporting

confidence: 77%

Differential molecular mechanism of docetaxel–octreotide combined treatment according to the docetaxel-resistance status in PC3 prostate cancer cells

et al. 2013

View full text Add to dashboard Cite

show abstract

“…39 However, longer exposure to the SST ligand and its analogs can restore SSTRs functions and surface levels. 39,40 Moreover, the ratio of internalized SSTRs to membranous SSTRs varies from one patient to the other, mainly due to active circulation of SSTRs regulated by various factors. 41 We examined the fiber knob-modified Ad5 vectors in the newly developed human blood loop model.…”

Section: Oncolytic Adenovirus With Somatostatin Motifs J Leja Et Almentioning

confidence: 99%

Oncolytic adenovirus modified with somatostatin motifs for selective infection of neuroendocrine tumor cells

Leja

Nilsson

et al. 2011

Gene Ther

View full text Add to dashboard Cite

We have previously described the oncolytic adenovirus, Ad(CgA-E1A-miR122), herein denoted Ad5(CgA-E1A-miR122) that selectively replicates in and kills neuroendocrine cells, including freshly isolated midgut carcinoid cells from liver metastases. Ad5(CgA-E1A-miR122) is based on human adenovirus serotype 5 (Ad5) and infects target cells by binding to the coxsackieadenovirus receptor (CAR) and integrins on the cell surface. Some neuroendocrine tumor (NET) and neuroblastoma cells express low levels of CAR and are therefore poorly transduced by Ad5. However, they often express high levels of somatostatin receptors (SSTRs). Therefore, we introduced cyclic peptides, which contain four amino acids (FWKT) and mimic the binding site for SSTRs in the virus fiber knob. We show that FWKT-modified Ad5 binds to SSTR 2 on NET cells and transduces midgut carcinoid cells from liver metastases about 3-4 times better than non-modified Ad5. Moreover, FWKT-modified Ad5 overcomes neutralization in an ex vivo human blood loop model to greater extent than Ad5, indicating that fiber knob modification may prolong the systemic circulation time. We conclude that modification of adenovirus with the FWKT motif may be beneficial for NET therapy.

show abstract

“…These contrary results may be due to the different cell characteristics, expression of the receptor and their subtypes and a high OCT treatment concentration. Furthermore, mRNA is not reliable as an index to reflect the status of the receptor, and we should therefore focus on the cell membrane localized receptor protein (19). The SSTR expression in ovarian cancer cells and the mechanism of the inhibitory effects of OCT on proliferation merit further study.…”

Section: Discussionmentioning

confidence: 99%

Octreotide enhances the sensitivity of the SKOV3/DDP ovarian cancer cell line to cisplatin chemotherapy in vitro

Shen¹,

Ren²,

Shi³

et al. 2011

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. The present study aimed to investigate the effects of octreotide (OCT) on the reversal of resistance of cisplatin-resistant cancer cells and on enhancement of the cisplatin sensitivity of cancer cells. The 3-(4,5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide method and flow cytometry were used to investigate the effect of cisplatin, OCT or the combination of these two compounds on the proliferation and apoptosis of SKOV3/DDP cells. Real-time, quantitative RT-PCR was used to detect the mRNA expression of SSTR2, MDR1, MRP2, GST-π and EGFR in SKOV3/DDP cells following OCT treatment. At the concentration of 2.5-20 µg/ml, OCT significantly reduced the IC 50 value (P<0.05) and promoted apoptosis (P<0.05) in the SKOV3/DDP cells in response to cisplatin. The synergistic effect of OCT and cisplatin on SKOV3/DDP cell proliferation was observed. SSTR2 was expressed on the SKOV3/DDP cell surface. OCT increased GST-π expression (P<0.05) and reduced MRP2 and EGFR expression (P<0.05) in a dose-dependent manner. However, it had no effect on the expression of MDR1 (P>0.05). It is suggested that OCT inhibits ovarian cancer proliferation and promotes apoptosis, via the cell surface expression of SSRT2, and reverses cisplatin resistance through the inhibition of MRP2 and EGFR expression.

show abstract

Mechanisms and Influence of Octreotide-Induced Regulation of Somatostatin Receptor 2 on Hepatocellular Carcinoma

Cited by 23 publications

References 38 publications

Differential molecular mechanism of docetaxel–octreotide combined treatment according to the docetaxel-resistance status in PC3 prostate cancer cells

Differential molecular mechanism of docetaxel–octreotide combined treatment according to the docetaxel-resistance status in PC3 prostate cancer cells

Oncolytic adenovirus modified with somatostatin motifs for selective infection of neuroendocrine tumor cells

Octreotide enhances the sensitivity of the SKOV3/DDP ovarian cancer cell line to cisplatin chemotherapy in vitro

Contact Info

Product

Resources

About