Non-digestible carbohydrates supplementation increases miR-32 expression in the healthy human colorectal epithelium: A randomized controlled trial.
Non-digestible carbohydrates supplementation increases miR-32 expression in the healthy human colorectal epithelium: A randomized controlled trial.
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不可消化的碳水化合物补充剂在健康的人类大肠上皮中增加了miR-32的表达:一项随机对照试验。
DOI:
10.1002/mc.22666
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发表时间:
2017-09
影响因子:
4.6
通讯作者:
Mathers JC
中科院分区:
文献类型:
--
作者:
Malcomson FC;Willis ND;McCallum I;Xie L;Lagerwaard B;Kelly S;Bradburn DM;Belshaw NJ;Johnson IT;Mathers JC
Colorectal cancer (CRC) risk is modulated by diet and there is convincing evidence of reduced risk with higher non‐digestible carbohydrates (NDCs) consumption. Resistant starch (RS), a NDC, positively modulates the expression of oncogenic microRNAs, suggesting that this could be a mechanism through which NDCs protect against CRC. The present study aimed to investigate the effects of supplementation with two NDCs, RS, and polydextrose (PD), on microRNA expression in the macroscopically‐normal human rectal epithelium using samples from the DISC Study, a randomized, double‐blind, placebo‐controlled dietary intervention. We screened 1008 miRNAs in pooled post‐intervention rectal mucosal samples from participants allocated to the double placebo group and those supplemented with both RS and PD. A total of 111 miRNAs were up‐ or down‐regulated by at least twofold in the RS + PD group compared with the control group. From these, eight were selected for quantification in individual participant samples by qPCR, and fold‐change direction was consistent with the array for seven miRNAs. The inconsistency for miR‐133b and the lower fold‐change values observed for the seven miRNAs is probably because qPCR of individual participant samples is a more robust and sensitive method of quantification than the array. miR‐32 expression was increased by approximately threefold (P = 0.033) in the rectal mucosa of participants supplemented with RS + PD compared with placebo. miR‐32 is involved in the regulation of processes such as cell proliferation that are dysregulated in CRC. Furthermore, miR‐32 may affect non‐canonical NF‐κB signaling via regulation of TRAF3 expression and consequently NIK stabilization.
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影响因子:
16
作者:
Donohoe, Dallas R.;Collins, Leonard B.;Wali, Aminah;Bigler, Rebecca;Sun, Wei;Bultman, Scott J.
通讯作者:
Bultman, Scott J.
影响因子:
2.9
作者:
Ma, Wenqi;Yu, Qiang;Zhou, Qi
通讯作者:
Zhou, Qi
影响因子:
3.7
作者:
Hu S;Dong TS;Dalal SR;Wu F;Bissonnette M;Kwon JH;Chang EB
通讯作者:
Chang EB
影响因子:
8.8
作者:
Diosdado B;van de Wiel MA;Terhaar Sive Droste JS;Mongera S;Postma C;Meijerink WJ;Carvalho B;Meijer GA
通讯作者:
Meijer GA
影响因子:
3.3
作者:
Humphreys, Karen J.;Conlon, Michael A.;Le Leu, Richard K.
通讯作者:
Le Leu, Richard K.