Endocrine gland-derived vascular endothelial growth factor modulates proliferation, apoptosis and migration in pancreatic cancer cells

Ren, Luping; Guo, Xiaozhong; Shao, Xiaodong; Li, Hongyu; Yao, Hui

doi:10.3892/mmr.2015.3340

Cited by 6 publications

(4 citation statements)

References 24 publications

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“…PROK-1 is secreted by cells in the placenta that promotes angiogenesis and capillary fenestration only in endocrine glands 27 28. Data from in vitro studies using normal and tumor cells show that PROK-1 and its receptor are present within the pancreas, which can stimulate proliferation and reduce apoptosis of endothelial cells 29 30. It was interesting that both IL-6 and GCG were elevated during later gestational ages, as animal studies have provided insights to the relationship between IL-6, GCG, and insulin secretion.…”

Section: Discussionmentioning

confidence: 99%

Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes

Espes

Magnusson

Caballero-Corbalan

et al. 2022

BMJ Open Diab Res Care

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IntroductionPregnancy entails both pancreatic adaptations with increasing β-cell mass and immunological alterations in healthy women. In this study, we have examined the effects of pregnancy on β-cell function and immunological processes in long-standing type 1 diabetes (L-T1D).Research design and methodsFasting and stimulated C-peptide were measured after an oral glucose tolerance test in pregnant women with L-T1D (n=17) during the first trimester, third trimester, and 5–8 weeks post partum. Two 92-plex Olink panels were used to measure proteins in plasma. Non-pregnant women with L-T1D (n=30) were included for comparison.ResultsFasting C-peptide was detected to a higher degree in women with L-T1D during gestation and after parturition (first trimester: 64.7%, third trimester: 76.5%, and post partum: 64.7% vs 26.7% in non-pregnant women). Also, total insulin secretion and peak C-peptide increased during pregnancy. The plasma protein levels in pregnant women with L-T1D was dynamic, but few analytes were functionally related. Specifically, peripheral levels of prolactin (PRL), prokineticin (PROK)-1, and glucagon (GCG) were elevated during gestation whereas levels of proteins related to leukocyte migration (CCL11), T cell activation (CD28), and antigen presentation (such as CD83) were reduced.ConclusionsIn summary, we have found that some C-peptide secretion, that is, an indirect measurement of endogenous insulin production, is regained in women with L-T1D during pregnancy, which might be attributed to elevated peripheral levels of PRL, PROK-1, or GCG.

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Section: Discussionmentioning

confidence: 99%

Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes

Espes

Magnusson

Caballero-Corbalan

et al. 2022

BMJ Open Diab Res Care

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“…Moreover, PROK1 was shown to be up-regulated in several types of cancers, such as colorectal cancer, pancreatic cancer, prostate cancer, and ovarian cancer [ 25 , 26 , 27 , 28 , 29 , 30 ], and was regarded as a poor prognostic marker and survival factor. These PROK1-related malignancies were closely associated with advanced clinical stage, histological grade, and distant metastasis, which may probably through regulating peritumoral angiogenesis or/and strengthened cancer cell invasiveness [ 25 , 26 , 27 , 28 , 29 , 30 ]. The PROK1-overexpressing cells in the present study could be a mimicking condition of malignancy, and the increased cell invasion ability suggested the potential role of PROK1 in cancer biology.…”

Section: Discussionmentioning

confidence: 99%

A Common Variant of PROK1 (V67I) Acts as a Genetic Modifier in Early Human Pregnancy through Down-Regulation of Gene Expression

Huang

Tsai

et al. 2016

IJMS

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PROK1-V67I has been shown to play a role as a modifier gene in the PROK1-PROKR system of human early pregnancy. To explore the related modifier mechanism of PROK1-V67I, we carried out a comparison study at the gene expression level and the cell function alternation of V67I, and its wild-type (WT), in transiently-transfected cells. We, respectively, performed quantitative RT-PCR and ELISA assays to evaluate the protein and/or transcript level of V67I and WT in HTR-8/SV neo, JAR, Ishikawa, and HEK293 cells. Transiently V67I- or WT-transfected HTR-8/SV neo and HEK293 cells were used to investigate cell function alternations. The transcript and protein expressions were down-regulated in all cell lines, ranging from 20% to 70%, compared with WT. There were no significant differences in the ligand activities of V67I and WT with regard to cell proliferation, cell invasion, calcium influx, and tubal formation. Both PROK1 alleles promoted cell invasion and intracellular calcium mobilization, whereas they had no significant effects on cell proliferation and tubal formation. In conclusion, the biological effects of PROK1-V67I on cell functions are similar to those of WT, and the common variant of V67I may act as a modifier in the PROK1-PROKR system through down-regulation of PROK1 expression. This study may provide a general mechanism that the common variant of V67I, modifying the disease severity of PROK1-related pathophysiologies.

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“…In this context, it has been shown that the PKS is associated with malignant carcinoma development [36]. In detail, PK1, an already known angiogenic factor, has been associated with tumorigenesis, cellular invasion, and metastases onset in several tumors [75][76][77][78], including CRC [65,79]. From these studies, which analyzed PK1 expression in human colorectal cancer tissue samples, it emerged that PK1 upregulation was present in about 40% of the CRC samples collected.…”

Section: Evidence Of the Pks In Gastrointestinal Tumorigenesis In Ibdsmentioning

confidence: 99%

The Prokineticin System in Inflammatory Bowel Diseases: A Clinical and Preclinical Overview

Amodeo,

Franchi,

Galimberti

et al. 2023

Biomedicines

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Inflammatory bowel disease (IBD) includes Crohn’s disease (CD) and ulcerative colitis (UC), which are characterized by chronic inflammation of the gastrointestinal (GI) tract. IBDs clinical manifestations are heterogeneous and characterized by a chronic relapsing-remitting course. Typical gastrointestinal signs and symptoms include diarrhea, GI bleeding, weight loss, and abdominal pain. Moreover, the presence of pain often manifests in the remitting disease phase. As a result, patients report a further reduction in life quality. Despite the scientific advances implemented in the last two decades and the therapies aimed at inducing or maintaining IBDs in a remissive condition, to date, their pathophysiology still remains unknown. In this scenario, the importance of identifying a common and effective therapeutic target for both digestive symptoms and pain remains a priority. Recent clinical and preclinical studies have reported the prokineticin system (PKS) as an emerging therapeutic target for IBDs. PKS alterations are likely to play a role in IBDs at multiple levels, such as in intestinal motility, local inflammation, ulceration processes, localized abdominal and visceral pain, as well as central nervous system sensitization, leading to the development of chronic and widespread pain. This narrative review summarized the evidence about the involvement of the PKS in IBD and discussed its potential as a druggable target.

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Endocrine gland-derived vascular endothelial growth factor modulates proliferation, apoptosis and migration in pancreatic cancer cells

Cited by 6 publications

References 24 publications

Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes

Pregnancy induces pancreatic insulin secretion in women with long-standing type 1 diabetes

A Common Variant of PROK1 (V67I) Acts as a Genetic Modifier in Early Human Pregnancy through Down-Regulation of Gene Expression

The Prokineticin System in Inflammatory Bowel Diseases: A Clinical and Preclinical Overview

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