Human pancreatic cancer cell proliferation in tissue culture is tonically inhibited by opioid growth factor.

Zagon, Ian S.; Smith, Jill P.; McLaughlin, Patricia J.

doi:10.3892/ijo.14.3.577

Cited by 49 publications

(81 citation statements)

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“…Log phase SK-HEP-1 and Hep G2 cells were plated onto 22-mm round cover glasses and cultured for 72 h. Frozen tissue samples were sectioned on a cryostat at 10 m and transferred to gelatin-coated slides. Cells and tissues were fixed and permeabilized in 95% EtOH and acetone and processed for immunohistochemistry, according to previously published procedures (2,27,(32)(33)(34). Polyclonal antibodies to OGF and OGFr were generated in the laboratory and have been fully characterized (31).…”

Section: Methodsmentioning

confidence: 99%

“…Attenuation of the OGF-OGFr axis in cancer cells through: 1) disruption of OGF-OGFr interfacing by continuous exposure to opioid antagonists [e.g., naltrexone (NTX)] (2, 15, 34), 2) neutralization of OGF by antibodies to the peptide (15), or 3) a decrease in OGFr by antisense cDNA or siRNA for OGFr (26,37), stimulates cell proliferation. An increase in OGF-OGFr activity in cancer cells by 1) addition of exogenous OGF (2,15,34); 2) treatment with imidazoquinoline compounds, such as imiquimod and resiquimod (26); or 3) transfection of sense cDNA for OGFr (18,35), depresses cell proliferation.…”

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confidence: 99%

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The opioid growth factor-opioid growth factor receptor axis regulates cell proliferation of human hepatocellular cancer

Avella¹,

Kimchi²,

Donahue

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

The opioid growth factor-opioid growth factor receptor axis regulates cell proliferation of human hepatocellular cancer

Avella¹,

Kimchi²,

Donahue

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The mechanism of action appears to be that OGF upregulates the cyclindependent kinase inhibitor pathway in order to delay the G 0 /G 1 phase of the cell cycle (14). OGF and OGFr have been demonstrated by immunohistochemistry, radioimmunoassay, and/or receptor binding to be present in a variety of human and animal tumors and cancer cell lines (1)(2)(3)(4)(5)8,(15)(16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

“…The opioid growth factor (OGF) ([Met 5 ]-enkephalin) and its receptor, OGFr, have been well documented in the regulation of growth of a variety of human cancer cells in culture (1)(2)(3)(4)(5) and tumors in nude mice (6)(7)(8)(9). OGF serves as an autocrineproduced, endogenous pentapeptide that inhibits cell proliferation in a receptor-mediated manner (1)(2)(3)(4)(5)10).…”

Section: Introductionmentioning

confidence: 99%

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Progression of squamous cell carcinoma of the head and neck is associated with down-regulation of the opioid growth factor receptor

McLaughlin

Zagon

2006

Int J Oncol

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Abstract. Opioid growth factor (OGF) is a native opioid peptide ([Met 5 ]-enkephalin) that interacts with the OGF receptor (OGFr). OGF serves as a tonically active negative growth factor in neoplasia, and the OGF-OGFr axis contributes to the maintenance of an equilibrium in cell proliferation by targeting the cyclin-dependent inhibitory kinase pathway. To inquire whether the expression of OGFr is related to tumor progression, cell lines of human squamous cell carcinoma of the head and neck (SCCHN) were transplanted into nude mice, and small, medium, and large tumors were assessed for OGFr by receptor binding assays and quantitative immunohistochemistry, and for gene expression of OGFr mRNA. Large tumors had a reduction of 3-to 7-fold in OGFr binding sites relative to small tumors, and medium size tumors showed a progressive diminishment in OGF receptors that ranged between that of small and large neoplasias. Tumors with xenografts of three different cell lines of SCCHN, representing poorly-and well-differentiated cancers, exhibited similar results. Quantitative densitometric immunohistochemistry revealed data comparable to receptor binding assays. Receptor affinity and the gene expression of OGFr mRNA were unchanged in tumors of different sizes. These data demonstrate that OGFr is reduced in SCCHN with tumor progression and that translation/ posttranslation of OGFr protein, but not transcriptional levels of the OGFr gene, is (are) involved. The attenuated levels of OGFr binding capacity may serve as a marker of SCCHN. These subnormal levels of OGFr may diminish the efficacy of the OGF-OGFr axis in maintaining cell proliferative activity, and contribute to more active cell replication. Gene therapy to reinstate more OGFr, and thus enhance OGFr function, could serve as a useful treatment for inhibiting tumor progression.

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Plasma cell‐free DNA methylome profiling in pre‐ and post‐surgery oral cavity squamous cell carcinoma

Patel

Padhya

Huang

et al. 2023

Molecular Carcinogenesis

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Head and neck squamous cell carcinoma (HNSCC), a highly heterogeneous disease that involves multiple anatomic sites, is a leading cause of cancer-related mortality worldwide. Although the utility of noninvasive biomarkers based on circulating cellfree DNA (cfDNA) methylation profiling has been widely recognized, limited studies have been reported so far regarding the dynamics of cfDNA methylome in oral cavity squamous cell carcinoma (OCSCC). It is hypothesized in this study that comparison of methylation profiles in pre-and postsurgery plasma samples will reveal OCSCC-specific prognostic and diagnostic biomarkers. As a strategy to further prioritize tumor-specific targets, top differential methylated regions (DMRs) were called by reanalyzing methylation data from paired tumor and normal tissue collected in the the cancer genome atlas head-neck squamous cell carcinoma (TCGA) head and neck cancer cohort. Matched plasma samples from eight patients with OCSCC were collected at Moffitt Cancer Center before and after surgical resection.Plasma-derived cfDNA was analyzed by cfMBD-seq, which is a high-sensitive methylation profiling assay. Differential methylation analysis was then performed based on the matched samples profiled. In the top 200 HNSCC-specific DMRs detected based on the TCGA data set, a total of 23 regions reached significance in the plasma-based DMR test. The top five validated DMR regions (ranked by the significance in the plasma study) are located in the promoter regions of genes PENK, NXPH1, ZIK1, TBXT, and CDO1, respectively. The genome-wide cfDNA DMR analysis further highlighted candidate biomarkers located in genes SFRP4, SOX1, IRF4, and PCDH17. The prognostic relevance of candidate genes was confirmed by survival analysis using the TCGA data. This study supports the utility of cfDNA-based methylome profiling as a promising noninvasive biomarker source for OCSCC and HNSCC.

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Human pancreatic cancer cell proliferation in tissue culture is tonically inhibited by opioid growth factor.

Cited by 49 publications

References 0 publications

The opioid growth factor-opioid growth factor receptor axis regulates cell proliferation of human hepatocellular cancer

The opioid growth factor-opioid growth factor receptor axis regulates cell proliferation of human hepatocellular cancer

Progression of squamous cell carcinoma of the head and neck is associated with down-regulation of the opioid growth factor receptor

Plasma cell‐free DNA methylome profiling in pre‐ and post‐surgery oral cavity squamous cell carcinoma

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