Vitamin D, linoleic acid, arachidonic acid and COX-2 in colorectal cancer patients in relation to disease stage, tumour localisation and disease progression

Berska, Joanna; Bugajska, Jolanta; Agnieszka, Grabowska; Hodorowicz-Zaniewska, Diana; Sztefko, Krystyna

doi:10.1016/j.ajg.2019.05.007

Cited by 10 publications

(9 citation statements)

References 39 publications

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“…In C3H/HeN mice, hepatic contents of free ARA, an endogenous lipid that is a structural isomer of GGA, did not decrease with aging, but rather increased in tumor tissue (unpublished results). The increase in ARA in tumor tissue observed here is consistent with previous studies showing that ARA acts as an inflammatory mediator via eicosanoids [28,29] . In other words, it can be considered hepatic fatty acid synthesis does not decrease in general with aging of C3H/HeN mice, and endogenous GGA levels specifically decreased in C3H/HeN mouse liver, which is probably due to a decrease in the GGA biosynthesis.…”

Section: Discussionsupporting

confidence: 93%

Age-dependent decrease of hepatic geranylgeranoic acid and its oral supplementation prevents spontaneous hepatoma in C3H/HeN mice

Tabata

Omori

Shidoji

2021

Preprint

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Aim: Geranylgeranoic acid (GGA) has been developed as a preventive agent against second primary hepatoma. Recently, GGA was reported to induce cell death in human hepatoma cells via TLR4-mediated pyroptosis. We have reported that GGA is enzymatically biosynthesized from mevalonic acid in human hepatoma-derived cells and that endogenous GGA is found in most organs of rats. In addition, we found that upregulation of endogenous GGA levels by zaragozic acid A (ZAA) induced cell death in human hepatoma-derived cells. Therefore, we investigated the age-related changes of hepatic GGA and the possibility of suppressing hepatocarcinogenesis by GGA supplementation using male C3H/HeN mice that spontaneously develop hepatoma. Methods: We measured endogenous GGA and mRNA of MAOB, a key enzyme of GGA biosynthesis, in the liver of male C3H/HeN mice aged 6-93 weeks. We also tried suppressing spontaneous hepatocarcinogenesis by a single administration of GGA to C3H/HeN mice. Results: Hepatic GGA content and Maob mRNA expression level age-dependently decreased in male C3H/HeN mice, some of which produced spontaneous hepatoma in 2 years. A single oral administration of GGA at 11 months of age significantly prevented hepatoma in terms of the number and weight of tumors per mouse at 23 months. Oral supplementation with GGA or geranylgeraniol significantly increased endogenous hepatic GGA contents dose-dependently, and ZAA dramatically upregulated hepatic GGA. Conclusion: In this study, we found an age-dependent decrease in hepatic endogenous GGA in male C3H/HeN mice and efficient prevention of spontaneous hepatoma by a single administration of GGA at 11 months of age.

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Section: Discussionsupporting

confidence: 93%

Age-dependent decrease of hepatic geranylgeranoic acid and its oral supplementation prevents spontaneous hepatoma in C3H/HeN mice

Tabata

Omori

Shidoji

2021

Preprint

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“…Several studies demonstrate an inverse correlation between colorectal cancer and 25VD levels [58,59]. The findings do not correspond to the results of a larger Vitamin D Deficiency study, detecting no significant association between colorectal cancer and VD status [60].…”

Section: Colorectal Cancermentioning

confidence: 66%

Vitamin D Deficiency in Renal Disease

Filipov¹,

Dimitrov²

2020

Vitamin D Deficiency

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Vitamin D deficiency is highly prevalent in patients with renal disease. The abnormal vitamin D (VD) metabolism in chronic kidney disease (CKD) is a key factor for developing CKD-related mineral bone disease (CKD-MBD), which directly influences the survival of the CKD patients. The importance of VD is perhaps of greater value due to its pleiotropic effects that span beyond calcium-phosphorus metabolism (cancer protection, diabetes prevention, and renal protection). The aim of our chapter is to depict the clinical implications of VD deficiency in the setting of CKD, including VD pleiotropy in renal disease, and to propose the most adequate treatment suggested in the literature. Keywords: vitamin D deficiency, chronic kidney disease, mineral bone disease, vitamin D pleiotropy, vitamin D supplementationVitamin D Deficiency 2 the ratio between free and total 25VD remained unchained; therefore, total 25VD is the indicator of VD status in CKD [3].Generally, 25VD level has reverse association with parathyroid hormone (PTH) levels. In addition, higher 25VD is associated with higher calcium intestinal reabsorption. However, at 25VD ≥ 75 nmol/l, no reduction in PTH levels and no increase in calcium intestinal reabsorption occurs [4, 5]. Therefore, 25VD ≥ 75 nmol/l is regarded as a cut-off value for vitamin D sufficiency.No generally accepted definition for VD deficiency exists, as authors choose cut-off value either serum 25VD of 25 nmol/L [6] or serum 25VD of 50 nmol/L [7]. However, target levels of 75 nmol/L are recommended, taking into consideration the clinical importance of mild VD insufficiency (25VD between 50 and 74.9 nmol/L) [7,8].Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, present for more than 3 months, with implications for health [one of the following: estimated glomerular filtration rate (eGFR) less than 60 ml/ min/1.73 m 2 ,presence of proteinuria, structural abnormalities of the kidney detected on imaging, pathological findings detected on kidney biopsy, urine sediment pathology, electrolyte abnormalities due to tubular disorders, history of kidney transplantation] [9]. CKD patients are at increased risk for VD deficiency; therefore, they require VD screening [7]. Vitamin D metabolism in health and renal disease VD metabolism in healthy subjectsVD is synthesized predominantly endogenously (approx. to 90% of the total VD in human body). In the skin, the ultraviolet light transforms 7-dehydroxycholesterol (provitamin D) to pre-vitamin D, which under the influence of body temperature spontaneously isomerizes to cholecalciferol (vitamin D3). Approximately, 10% of total body VD is taken orally (vitamin D2, ergocalciferol, and cholecalciferol). VD is transported via VD-binding protein to the liver, where it is hydroxylated to 25VD. The next step in VD activation is hydroxylation of 25VD by the enzyme 1α-hydroxylase (CYP27B1) to 1,25VD, which is the active VD metabolite. The process occurs predominantly in the renal tubules. In addition, non-renal CYP27B1 was detected...

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“…Previous studies have revealed that vitamin d, which can be hydroxylated to the active form 1,25(oH) 2 d3 (referred to as vitamin d or d3 in the present study), activates Vdr (9,10). Furthermore, Vdr expression is associated with cancer risk and mortality in various types of cancer, including breast, lung and colorectal cancer (11)(12)(13)(14). other studies suggested that the vitamin d and Vdr complex binds to p21 and p27 proteins, which suppress dna synthesis, inactivate mitogenic signals and inhibit tumor progression (15)(16)(17)(18).…”

Section: Introductionmentioning

confidence: 64%

“…Vitamin D is synthesized through a series of steps, starting from a cholesterol precursor molecule that is transformed into the vitamin D hormone precursor (vitamin D 3 ) and subsequently hydroxylated to its most active hormone form, 1,25(OH) 2 D3, in the liver and kidney ( 14 ). Vitamin D binds to VDR when it enters the cells, forming a complex that is reported to influence cell cycle regulation by decreasing DNA synthesis, inactivating mitogenic signals, reducing expression of c-Myc and inhibiting cell differentiation, which inhibit tumor formation in several types of cancer, including breast, colorectal and lung cancer ( 13 , 28 , 29 ). For example, in breast cancer, vitamin D modulates the intracellular kinase pathways (including p38 mitogen activated protein kinase and ERK), represses the expression of proto-oncogenes (such as c-Myc) and decreases the proliferation of breast cancer cells ( 15 , 30 ).…”

Section: Discussionmentioning

confidence: 99%

Vitamin D receptor knockdown attenuates the antiproliferative, pro‑apoptotic and anti‑invasive effect of vitamin D by activating the Wnt/β‑catenin signaling pathway in papillary thyroid cancer

Pang

et al. 2020

Mol Med Rep

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Vitamin d and the vitamin d receptor (Vdr) complex have been reported to inhibit the growth of several types of tumor; however, their function in papillary thyroid cancer (PcT) remains unknown. in addition, the Wnt/β-catenin signaling pathway was discovered to serve a critical role in the pathology of PcT. Therefore, the present study aimed to determine the role of the Vdr and its association with Wnt/β-catenin signaling in vitamin d-treated PTc cells. Vdr expression was detected in human PTc cells (including Mda-T120, Mda-T85, Snu-790 and iHH4 cells) and thyroid follicular cells (nthy-ori 3-1 cells). Snu-790 and iHH4 cells were infected with Kd-Vdr or negative control (Kd-nc) lentiviruses, treated with 1,25(oH) 2 d3 (the active form of vitamin d), and subsequently referred to as the Kd-Vdr&vitd and Kd-nc&vitd groups, respectively. additionally, PTc cells infected with Kd-nc and not treated with 1,25(oH) 2 d3 were used as the normal control and referred to as the Kd-nc group. Vdr mrna and protein expression levels were increased in Mda-T120, Snu-790 and Mda-T85 cells compared to nthy-ori 3-1 cells, whereas in iHH4 cells, Vdr mrna and protein expression levels were similar to nthy-ori 3-1 cells. in Snu-790 and iHH4 cells, cell proliferation and invasion were decreased in the Kd-nc&vitd group compared with the Kd-nc group, but increased in the Kd-Vdr&vitd group compared with the Kd-nc&vitd group. cell apoptosis was increased in the Kd-nc&vitd group compared with the Kd-nc group, and decreased in the Kd-Vdr&vitd group compared with the Kd-nc&vitd group. Furthermore, the expression levels of Wnt family member 3 and catenin β1 were decreased in the Kd-nc&vitd group compared with the Kd-nc group, but increased in the Kd-Vdr&vitd group compared with the Kd-nc&vitd group. in conclusion, the present study revealed that Vdr-Kd attenuated the antiproliferative, pro-apoptotic and anti-invasive effects of vitamin d in PTc by activating the Wnt/β-catenin signaling pathway.

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Vitamin D, linoleic acid, arachidonic acid and COX-2 in colorectal cancer patients in relation to disease stage, tumour localisation and disease progression

Cited by 10 publications

References 39 publications

Age-dependent decrease of hepatic geranylgeranoic acid and its oral supplementation prevents spontaneous hepatoma in C3H/HeN mice

Age-dependent decrease of hepatic geranylgeranoic acid and its oral supplementation prevents spontaneous hepatoma in C3H/HeN mice

Vitamin D Deficiency in Renal Disease

Vitamin D receptor knockdown attenuates the antiproliferative, pro‑apoptotic and anti‑invasive effect of vitamin D by activating the Wnt/β‑catenin signaling pathway in papillary thyroid cancer

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