Opioid growth factor and the treatment of human pancreatic cancer: A review

Zagon, Ian S.

doi:10.3748/wjg.v20.i9.2218

Cited by 34 publications

(26 citation statements)

References 45 publications

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“…Though these neuropeptides are primarily known for their opioid activities due to their high affinity toward specific opioid receptors,[ 9 ] Met-Enk has been identified as an inhibitory growth factor in cancer and wound healing. [ 10 ] Due to its unique cell growth regulation properties, in addition to the classic agonist activities toward mu-opioid (MOP) and delta-opioid (DOP) receptor subtypes, this pentapeptide (Tyr–Gly–Gly–Phe–Met) is termed as opioid growth factor (OGF). [ 11 ] OGF functions in direct combination with its receptor, the opioid growth factor receptor (OGFr).…”

Section: Resultsmentioning

confidence: 99%

“…OGFrs are found to be overexpressed in the nuclear membranes of several cancer cells and immune cells such as T-cells, macrophages, and dendritic cells. [ 10 ] It has been shown that there is an elevated level of Met-Enk in the plasma of cancer patients, suggesting their functional roles in such disease states. [ 11 ] This is particularly true in the case of human pancreatic cancer in which both OGF and OGFr have been detected at higher levels.…”

Section: Resultsmentioning

confidence: 99%

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Lipid‐Conjugation of Endogenous Neuropeptides: Improved Biotherapy against Human Pancreatic Cancer

Gopalakrishnan

Lepetre

Maksimenko

et al. 2015

Adv Healthcare Materials

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Neuropeptides are small neuronal signaling molecules that act as neuromodulators for a variety of neural functions including analgesia, reproduction, social behavior, learning, and memory. One of the endogenous neuropeptides—Met-Enkephalin (Met-Enk), has been shown to display an inhibitory effect on cell proliferation and differentiation. Here, a novel lipid-modification approach is shown to create a small library of neuropeptides that will allow increased bioavailability and plasma stability after systemic administration. It is demonstrated, on an experimental model of human pancreatic adenocarcinoma, that lipid conjugation of Met-Enk enhances its tumor suppression efficacy compared to its nonlipidated counterparts, both in vitro and in vivo. More strikingly, the in vivo studies show that a combination therapy with a reduced concentration of Gemcitabine has suppressed the tumor growth considerably even three weeks after the last treatment.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Lipid‐Conjugation of Endogenous Neuropeptides: Improved Biotherapy against Human Pancreatic Cancer

Gopalakrishnan

Lepetre

Maksimenko

et al. 2015

Adv Healthcare Materials

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“…In this regard, the attainment of cardiogenesis in the presence of either chemical agents or physical stimulation encompasses the transcription and protein expression of endorphin peptides [33]. These molecules, besides their role in cardiogenesis [55][56][57], have long been shown to act as negative regulators for the development and spreading of different types of cancer [82][83][84][85][86][87].…”

Section: Cancer Stem Cells: Foe or Reprogrammable Cells For Efficientmentioning

confidence: 99%

Cancer Stem Cells: Foe or Reprogrammable Cells for Efficient Cancer Therapy?

Ventura¹,

Olivi²,

Cavallini³

et al. 2015

NanoWorld J

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Embryonic development and carcinogenesis share many molecular pathways and regulatory molecules. While the induction of a pluripotent state involves a significant oncogenic risk, as in induced pluripotent stem cells (iPSCs), the embryonic environment in vivo has been shown to suppress tumor development. In this review, we discuss the subtle equilibrium between the nanotopography (niche) of the hosting tissue resident stem cells and their biological dynamics, including the transformation in cancer stem cells. We review consistent findings indicating the potential for modulating the biology of human cancer stem cells by the aid of naturally occurring or synthetic molecules, including developmental stage zebrafish embryo extracts, hyaluronan, butyric acid (BA) and retinoic acid (RA), hyaluronan mixed esters of BA and RA, melatonin, vitamin D3, and endorphin peptides. Within this context, we dissect the multifaceted mechanisms orchestrated by endorphinergic systems, including paracrine cellto-cell communication, as well as the establishment of autocrine and intracrine (intracellular) peptide actions driving transcriptional responses and self-sustaining loops that behave as long-lived signals imparting features characteristic of differentiation, growth regulation and cell memory.Based upon the remarkable action of electromagnetic fields and mechanical vibration on (stem) cell signaling, differentiation, and senescence, we also consider the potential for using these physical energies as a tool to afford a fine tuning of cancer stem cell fate.On the whole, we forecast future deployment of the physical and/or chemical approaches described herein aiming at reprogramming, rather than destroying cancer stem cells, eventually placing cancer therapy within the context of Regenerative Medicine.

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“… 2 Data from previously published results from our laboratory indicated that MENK, in a dose-dependent manner, can inhibit tumor growth in vivo and in vitro. These studies have focused on human melanoma cancer, 10 human pancreatic cancer, 19 human ovarian cancer, 20 , 21 thyroid follicular cell-derived cancers, 22 human hepatocellular cancer, 23 and triple-negative breast cancer. 24 Our team has also demonstrated that MENK can inhibit human melanoma cancer cell growth by inducing cell apoptosis and cell cycle arrest in G0/G1 phase.…”

Section: Introductionmentioning

confidence: 99%

The novel mechanism of anticancer effect on gastric cancer through inducing G0/G1 cell cycle arrest and caspase-dependent apoptosis in vitro and in vivo by methionine enkephalin

Wang¹,

Tian²,

Jiao³

et al. 2018

CMAR

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BackgroundGastric cancer (GC) is the second cause of cancer-related deaths. Methionine enkephalin (MENK), an endogenous opioid peptide, has immunological and antitumor activity.PurposeThe aim of this work was to investigate whether MENK could exhibit activity against human GC in vitro and in vivo.Materials and methodsHuman GC cells were treated with MENK. Cell viability, colony formation, cell morphology, cell cycle, and apoptosis were assessed. The effects of MENK on gene expression of OGFr, Bax, BCL-2, caspase-3, PARP, Ki67, cyclin D1, c-myc, survivin were quantifed by qRT-PCR. Western blot was used to analyze the effects of MENK on protein expression of OGFr, Bax, BCL-2, caspase-3, PARP. The anti-tumor activity of MENK in gastic carcinoma was also investigated with animal experiments.ResultsThe results indicate that MENK could significantly inhibit the growth of human GC cells SGC7901 and HGC27 in a concentration- and time-dependent manner, decrease the number of cell colonies, and arrest cell cycle in the G0/G1 phase by causing a decrease in Ki67, cyclin D1, and c-myc mRNA. Furthermore, MENK could induce tumor cell apoptosis associated with the upregulation of Bax, a corresponding downregulation of BCL-2 and survivin, and activation of caspase-3 and PARP. Moreover, MENK upregulated the expression of opioid receptors (OGFr) in SGC7901 and HGC27 cells. The interaction between MENK and OGFr in SGC7901 and HGC27 cells appears to be essential for the antitumor activity of MENK.ConclusionWe conclude that MENK may be a potential drug for the treatment of GC.

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Opioid growth factor and the treatment of human pancreatic cancer: A review

Cited by 34 publications

References 45 publications

Lipid‐Conjugation of Endogenous Neuropeptides: Improved Biotherapy against Human Pancreatic Cancer

Lipid‐Conjugation of Endogenous Neuropeptides: Improved Biotherapy against Human Pancreatic Cancer

Cancer Stem Cells: Foe or Reprogrammable Cells for Efficient Cancer Therapy?

The novel mechanism of anticancer effect on gastric cancer through inducing G0/G1 cell cycle arrest and caspase-dependent apoptosis in vitro and in vivo by methionine enkephalin

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