Possible Molecular Mechanisms by which Vitamin D Prevents Inflammatory Bowel Disease and Colitis-associated Colorectal Cancer

Luan, Zijian; Yu, Xuezhong; Qian, Jiaming; Wang, Hongying

doi:10.2174/0929867323666161202153028

Cited by 7 publications

(7 citation statements)

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“…In the present study, we found that up‐regulation of CST5 could inhibit the serum levels of TRAP, BALP and OC of rats with OP yet promote the expression of CD61 on the surface of osteoclasts. The role of CST5 was previously revealed in colorectal cancer, in which loss of CST5 promoted tumour differentiation while induction of CST5 exerted a tumour‐suppressive effect on colorectal cancer . More importantly, as a cysteine proteinase inhibitor, CST5 could restrain osteoclast formation through interference of late‐staged differentiation of pre‐osteoclasts .…”

Section: Discussionmentioning

confidence: 91%

“…The role of CST5 was previously revealed in colorectal cancer, in which loss of CST5 promoted tumour differentiation while induction of CST5 exerted a tumoursuppressive effect on colorectal cancer. 11,26 More importantly, as a cysteine proteinase inhibitor, CST5 could restrain osteoclast formation through interference of late-staged differentiation of preosteoclasts. 21 TRAP was known to be an osteoclast marker, and the increased expression of TRAP was exhibited in osteoblasts and osteocytes in experimental OP rats.…”

Section: Discussionmentioning

confidence: 99%

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Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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Here, we aim at exploring the effect of CST5 on bone resorption and activation of osteoclasts in osteoporosis (OP) rats through the NF‐κB pathway. Microarray analysis was used to screen the OP‐related differentially expressed genes. Osteoporosis was induced in rats by intragastric retinoic acid administration. The serum levels of tartrate‐resistant acid phosphatase (TRAP), bone alkaline phosphatase (BALP) and osteocalcin (OC) and the expression of CD61 on the surface of osteoclasts were examined. The number of osteoclasts and the number and area of resorption pits were detected. Besides, the pathological changes and bone mineral density in bone tissues of rats were assessed. Also, the relationship between CST5 and the NF‐κB pathway was identified through determining the expression of CST5, RANKL, RANK, OPG, p65 and IKB. Poorly expressed CST5 was indicated to affect the OP. CST5 elevation and inhibition of the NF‐κB pathway decreased serum levels of TRAP, BALP and OC and expression of CD61 in vivo and in vitro. In OP rats, CST5 overexpression increased trabecular bones and bone mineral density of bone tissues, but decreased trabecular separation, fat within the bone marrow cavities and the number of osteoclasts through inhibiting the NF‐κB pathway. In vivo experiments showed that CST5 elevation inhibited growth in number and area of osteoclastic resorption pits and restrained osteoclastic bone absorption by inhibiting the NF‐κB pathway. In summary, overexpression of CST5 suppresses the activation and bone resorption of osteoclasts by inhibiting the activation of the NF‐κB pathway.

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Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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“…Wnt signaling is crucially involved in stem cell maintenance and epithelial cell proliferation [78][79][80]. Wnt is activated in most colon cancers; therefore, it can be used as a potential biomarker for colon health [78,81,82]. Wnt may also contribute to carcinogenesis from colitis to colon cancer [78,81,82].…”

Section: Wnt/β-cateninmentioning

confidence: 99%

“…Wnt is activated in most colon cancers; therefore, it can be used as a potential biomarker for colon health [78,81,82]. Wnt may also contribute to carcinogenesis from colitis to colon cancer [78,81,82]. Wnt is capable of signaling in a paracrine and autocrine manner, and the absence of Wnt promotes the degradation of β-catenin [79].…”

Section: Wnt/β-cateninmentioning

confidence: 99%

Effects of Vitamin D Supplementation on Inflammation, Colonic Cell Kinetics, and Microbiota in Colitis: A Review

et al. 2020

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Vitamin D is widely known to regulate bone health, but there is increasing evidence that it may also ameliorate colitis through inflammation, cell proliferation and apoptosis, and the microbiota. The purpose of this review is to systematically examine the mechanisms by which vitamin D reduces colitis. PubMed and Web of Science were searched for articles published between 2008 and 2019 using key words such as “vitamin D,” “colitis,” “inflammatory bowel disease,” “inflammation,” “apoptosis,” “cell proliferation,” and “gut bacteria”. Retrieved articles were further narrowed and it was determined whether their title and abstracts contained terminology pertaining to vitamin D in relation to colitis in human clinical trials, animal studies, and cell culture/biopsy studies, as well as selecting the best match sorting option in relation to the research question. In total, 30 studies met the established criteria. Studies consistently reported results showing that vitamin D supplementation can downregulate inflammatory pathways of COX-2, TNF-α, NF-κB, and MAPK, modify cell kinetics, and alter gut microbiome, all of which contribute to an improved state of colitis. Although vitamin D and vitamin D analogs have demonstrated positive effects against colitis, more randomized, controlled human clinical trials are needed to determine the value of vitamin D as a therapeutic agent in the treatment of colitis.

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“… 72 A large number of published studies have found that vitamin D can exert a key role in decreasing cancer risk. 17 – 19 , 73 – 75 The antitumor effects of vitamin D have been well established in several cancers, such as colorectal cancer and bladder cancer. 18 , 19 On the contrary, some studies found that vitamin D did not exert an antitumor effect in prostate cancer but even caused elevated risk of prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

Circulating vitamin D concentration and risk of prostate cancer: a dose–response meta-analysis of prospective studies

Gao¹,

Wei²,

Wang³

et al. 2018

TCRM

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BackgroundThough many studies have been performed to elucidate the association between circulating vitamin D and prostate cancer, no conclusive result is available. We carried out a dose–response meta-analysis to quantitatively examine the association of circulating 25-hydroxyvitamin D (25[OH]D) concentration with prostate cancer.MethodsOnly prospective studies examining the associations of circulating 25[OH]D concentration with prostate cancer were eligible for the meta-analysis. A random-effect meta-analysis was done first, to calculate the summary relative risk (RR) and 95% confidence intervals (CIs) comparing the higher concentration with the lower concentration of 25[OH]D. A dose–response meta-analysis using random-effects model was then carried out to evaluate the nonlinearity and calculate the summary RR caused per 10 ng/mL increment.ResultsNineteen prospective cohort or nested case–control studies were included. Higher 25[OH]D concentration was significantly correlated with elevated risk of prostate cancer (RR =1.15, 95% CI 1.06–1.24). No nonlinear relationship was found between 25[OH]D concentration and risk of prostate cancer (P=0.654). Dose–response meta-analysis showed that the summary RR caused per 10 ng/mL increment in circulating 25[OH]D concentration was 1.04 (95% CI 1.02–1.06). Subgroup analysis also found a modest dose–response relationship. Funnel plot and Egger’s test did not detect publication bias.ConclusionThe findings suggest that highest 25[OH]D concentration is correlated with elevated risk of prostate cancer and a modest dose–response effect exists in this association; however, more studies are needed.

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Possible Molecular Mechanisms by which Vitamin D Prevents Inflammatory Bowel Disease and Colitis-associated Colorectal Cancer

Cited by 7 publications

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Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Effects of Vitamin D Supplementation on Inflammation, Colonic Cell Kinetics, and Microbiota in Colitis: A Review

Circulating vitamin D concentration and risk of prostate cancer: a dose–response meta-analysis of prospective studies

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Possible Molecular Mechanisms by which Vitamin D Prevents Inflammatory Bowel Disease and Colitis-associated Colorectal Cancer

Cited by 7 publications

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Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Effects of Vitamin D Supplementation on Inflammation, Colonic Cell Kinetics, and Microbiota in Colitis: A Review

Circulating vitamin D concentration and risk of prostate cancer: a dose&ndash;response meta-analysis of prospective studies

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Circulating vitamin D concentration and risk of prostate cancer: a dose–response meta-analysis of prospective studies