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Vitamin D deficiency is associated with the risk of several common cancers.
The strongest evidence is the link between vitamin D and colorectal cancer (CRC)
.
However, causality has not yet been proven convincingly, because the existing observational evidence may be affected by several potential confounding factors
Vitamin D deficiency is associated with the risk of several common cancers.
A recent randomized controlled trial (RCT) reported an association between vitamin D supplementation, vitamin D receptor genotype, and RCR risk, supporting that beneficial effects may be a prerequisite for causality
According to reports, compared with normal colorectal tissues, CRC and adenoma tissues have different gene expressions, and genes involved in metabolism, transcription and translation, and cellular processes have generally changed
.
Therefore, in the case of vitamin D status or supplementary investigation colorectal gene expression might be the relationship between the CRC and vitamin D provide new insights
Survey colorectal gene expression might be the relationship between the CRC and vitamin D provide new insights in the case of vitamin D status or supplement
To determine whether oral vitamin D induces the expression of the effect of human colorectal epithelial cells of beneficial genes, and indeed given reaction biomarkers, experts from the Center for Tumor UK University of Edinburgh carried out the research, published in the latest BMC Medicine magazine
.
The researchers sampled the blood and rectal mucosa of 191 subjects, and correlated mucosal gene expression (HT12) with plasma vitamin D (25-OHD) to identify different expressed genes
.
Then 50 subjects were given 3200 IU/day vitamin D3 orally, and the matching blood/mucosa was resampled after 12 weeks
Simplified experimental design
Subsequently, the transcriptome changes (HT12/RNAseq) after vitamin D supplementation were detected
.
To determine the blood biomarkers of mucosal response, the researchers performed AUC curve plotting and tested the reproducibility of the biomarkers in an independent supplementary test (BEST-D)
The results showed that 629 genes were related to 25-OHD levels, and 453 of them were significant in GO-term process
.
In the entire intervention cohort, vitamin D supplementation enriched the priority mucosal genomes and corresponding GO pathways, highlighting gene expression patterns consistent with anti-tumor effects
In the entire intervention cohort, vitamin D supplementation enriched the priority mucosal genomes and corresponding GO pathways, highlighting gene expression patterns consistent with anti-tumor effects
In the SCOVIDS and BEST-D trials, the expression of HIPK2 and PPP1CC in blood before and after supplementation, and the ROC curve of biomarker utility
However, only 9 participants (18%) showed a clear response to nutritional supplements
.
The expression changes of HIPK2 and PPP1CC were used as blood biomarkers of mucosal transcriptome response (AUC=0.
The expression changes of HIPK2 and PPP1CC were used as blood biomarkers of mucosal transcriptome response (AUC=0.
84 [95%CI 0.
66-1.
00]), and were replicated in BEST-D test subjects (HIPK2 AUC=0.
83 [95%CI 0.
77 -0.
89]; PPP1CC AUC=0.
91 [95%CI 0.
86-0.
95])
.
The expression changes of HIPK2 and PPP1CC were used as blood biomarkers of mucosal transcriptome response (AUC=0.
84 [95%CI 0.
66-1.
00]), and were replicated in BEST-D test subjects (HIPK2 AUC=0.
83 [95%CI 0.
77 -0.
89]; PPP1CC AUC=0.
91 [95%CI 0.
86-0.
95])
.
In summary, higher plasma 25-OHD is related to rectal mucosal gene expression patterns, consistent with anti-tumor effects, and this beneficial feature is caused by short-term vitamin D supplementation
.
.
In summary, higher plasma 25-OHD is related to rectal mucosal gene expression patterns, consistent with anti-tumor effects, and this beneficial feature is caused by short-term vitamin D supplementation
.
references:
Oral vitamin D supplementation induces transcriptomic changes in rectal mucosa that are linked to anti-tumour effects.
BMC Med 19, 174 (2021).
https://doi.
org/10.
1186/s12916-021-02044-y
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