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

Shen, Yang; Ren, Mulan; Shi, Yao; Zhang, Yunxia; Cai, Yefeng

doi:10.3892/etm.2011.330

Cited by 15 publications

(15 citation statements)

References 24 publications

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“…A major clinical obstacle in cancer therapy is the development of resistance to a multitude of chemotherapeutic agents, a phenomenon called multidrug resistance (MDR) [10]. Therefore, the design of new therapies capable of reversing chemotherapy resistance and enhancing sensitivity to platinum-based chemotherapy drugs is critical [11]. …”

Section: Introductionmentioning

confidence: 99%

Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

et al. 2016

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BackgroundSialyltransferase I (ST6Gal-I) is an enzyme involved in tumor metastasis that processes sialic acid precursors into their mature form, enabling them to regulate gene expression. However, the effect of ST6Gal-I on the biological behavior of cancer cells remain unclear. This study was the first to demonstrate the influence of ST6Gal-I on cisplatin sensitivity in cervical cancer cells.MethodsKnockdown of ST6Gal-I was performed by shRNA and HeLa cells combination with cisplatin were tested.ResultsWe showed that down-regulation of ST6Gal-I promoted cell apoptosis and inhibited proliferation and invasion in cervical cancer cells. Knockdown of ST6Gal-I by RNA interference increased the sensitivity of HeLa cells to cisplatin in vitro, and reduced tumor volume and suppressed subcutaneous tumor growth in response to cisplatin treatment in a xenograft mouse model in vivo.ConclusionsThe results provide new information that ST6Gal-I plays an important role in several biological or pathological processes including drug resistance in cervical cancer and may be a potential therapeutic target to improve the response to chemotherapy in cervical cancer patients.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2981-y) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

et al. 2016

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“…We have seen the multiple extra-pituitary effects of octreotide by the number of genes involved in the immune response, cell differentiation, growth and maintenance affected by the analog (Table 2). Although studies examining the extra-pituitary actions of octreotide are limited, there are reports demonstrating octreotide inhibition of cyclin D1 ( Ccnd1 ) (Ferrante et al 2006) and epidermal growth factor receptor ( Egfr ) expression (Lai et al 2003, Shen et al 2011) as we too report.…”

Section: Discussionmentioning

confidence: 67%

Noncanonical suppression of GH-dependent isoforms of cytochrome P450 by the somatostatin analog octreotide

Das

Banerjee

Shapiro

2012

Journal of Endocrinology

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Octreotide is a potent somatostatin analog therapeutically used to treat several conditions including hyper growth hormone secretion in patients with acromegaly. We infused, over 30 sec, octreotide into male rats every 12 h for 6 days at levels considerably greater than typical human therapeutic doses. Unexpectedly, resulting circulating growth hormone profile were characterized by pulses of higher amplitudes, longer durations and greater total content than normal, but still contained an otherwise male-like episodic secretory profiles. In apparent disaccord, the normally elevated masculine expression levels (protein and/or mRNA) of CYP2C11 (accounting for >50% of the total hepatic cytochrome P450 content), CYP3A2, CYP2C7 and IGF1, all dependent on the episodic growth hormone profile, were considerably down-regulated. We explain this contradiction by proposing that the requisite minimal growth hormone-devoid interpulse durations in the masculine profile that solely regulate expression of at least CYP2C11 and IGF1 may be sufficiently reduced to suppress transcription of the hepatic genes. Alternatively, we observed that octreotide infusion may have acted directly on the hepatocytes to induce expression of immune response factors postulated to suppress CYP transcription and/or up-regulate expression of several negative regulators (e.g., phosphatases, SOCS proteins) of the JAK2/STAT5B signaling pathway that normally mediates the up-regulation of CYP2C11 and IGF1 by the masculine episodic growth hormone profile.

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“…Our earlier study showed that chemotherapy agent combined with OCT could markedly inhibit the proliferation and promote apoptosis of resistant ovarian cancer cells. This combination of the two single drugs has significant synergistic action (22,23). Furthermore, studies on synthesized POC in lung cancer cells have shown its cytotoxicity in vitro and in vivo (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

“…In previous studies, we detected the expression of SSTR2 in SKOV3/DDP by quantitative PCR and showed that OCT could inhibit ovarian cancer proliferation and promote apoptosis via the cell surface SSTR2. Furthermore, OCT could reverse cisplatin resistance through inhibition of MRP2, EGFR and GST-π expressions (22,23).…”

Section: Introductionmentioning

confidence: 99%

Synthetic paclitaxel-octreotide conjugate reverses the resistance of paclitaxel in A2780/Taxol ovarian cancer cell line

et al. 2016

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The high mortality of ovarian cancer is partly due to the frequent resistance of ovarian cancer to current chemotherapy agents such as paclitaxel and platinum. Somatostatin analogue (SSTA) has been shown to inhibit the proliferation of some tumors through binding to somatostatin receptor (SSTR) and activation of Ras-, Rapl- and B-Raf-dependent extracellular signal-regulated kinase 2 (Erk2). It was reported that paclitaxel-octreotide conjugate (POC) exhibited enhanced tumor growth inhibition with reduced toxicity. In the present study, we prepared the POC and investigated its effects and mechanism for the reversal of drug resistance in paclitaxel-resistant ovarian cancer cell line. We demonstrated that treatment with POC led to more cell apoptosis than either paclitaxel or octreotide (OCT) alone. Moreover, the expression of multidrug resistance 1 (MDR1) and vascular endothelial growth factor (VEGF) mRNA, and protein decreased in a dose-dependent manner while the expression of SSTR remained stable following treatment with POC. Although the exact action, in vivo effects and pharmacologic kinetics of POC remain to be investigated, we have demonstrated the feasibility for the synthesis of POC, and more significantly, provided a potential approach to overcome the resistance of ovarian cancer against taxol. The findings also shed some new light on the mechanisms underlying the development of resistance to taxol by ovarian cancer cells.

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

Cited by 15 publications

References 24 publications

Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

Noncanonical suppression of GH-dependent isoforms of cytochrome P450 by the somatostatin analog octreotide

Synthetic paclitaxel-octreotide conjugate reverses the resistance of paclitaxel in A2780/Taxol ovarian cancer cell line

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