Prognostic values of the miR‐17‐92 cluster and its paralogs in colon cancer

Guo, Yu; Tang, Jianqiang; Tian, Ming; Li, Hui; Wang, Xin; Wu, Tao; Zhu, Jing; Huang, Shenghui; Wan, Yao

doi:10.1002/jso.22138

Cited by 82 publications

(65 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The miR17-92 cluster has been designated oncomir-1 (31), and can promote proliferation and angiogenesis, inhibit differentiation, and sustain cell survival (29,30). Elevated miR17-92 levels have been associated with invasion and metastasis of colorectal cancer cells (32), and poorer survival (33). miR19a and miR19b in particular are key oncogenic determinants (29,30), and both were significantly elevated with the HRM diet compared with the entry diet.…”

Section: Discussionmentioning

confidence: 99%

Dietary Manipulation of Oncogenic MicroRNA Expression in Human Rectal Mucosa: A Randomized Trial

Humphreys

Conlon

Young

et al. 2014

Cancer Prevention Research

100

View full text Add to dashboard Cite

High red meat (HRM) intake is associated with increased colorectal cancer risk, while resistant starch is probably protective. Resistant starch fermentation produces butyrate, which can alter microRNA (miRNA) levels in colorectal cancer cells in vitro; effects of red meat and resistant starch on miRNA expression in vivo were unknown. This study examined whether a HRM diet altered miRNA expression in rectal mucosa tissue of healthy volunteers, and if supplementation with butyrylated resistant starch (HRMþHAMSB) modified this response. In a randomized cross-over design, 23 volunteers undertook four 4-week dietary interventions; an HRM diet (300 g/day lean red meat) and an HRMþHAMSB diet (HRM with 40 g/day butyrylated high amylose maize starch), preceded by an entry diet and separated by a washout. Fecal butyrate increased with the HRMþHAMSB diet. Levels of oncogenic mature miRNAs, including miR17-92 cluster miRNAs and miR21, increased in the rectal mucosa with the HRM diet, whereas the HRMþHAMSB diet restored miR17-92 miRNAs, but not miR21, to baseline levels. Elevated miR17-92 and miR21 in the HRM diet corresponded with increased cell proliferation, and a decrease in miR17-92 target gene transcript levels, including CDKN1A. The oncogenic miR17-92 cluster is differentially regulated by dietary factors that increase or decrease risk for colorectal cancer, and this may explain, at least in part, the respective risk profiles of HRM and resistant starch. These findings support increased resistant starch consumption as a means of reducing risk associated with an HRM diet. Cancer Prev Res; 7(8); 786-95. Ó2014 AACR.

show abstract

Section: Discussionmentioning

confidence: 99%

Dietary Manipulation of Oncogenic MicroRNA Expression in Human Rectal Mucosa: A Randomized Trial

Humphreys

Conlon

Young

et al. 2014

Cancer Prevention Research

100

View full text Add to dashboard Cite

show abstract

“…Alterations of miRs are crucial for tumorigenesis (11). miRs exhibit potential as diagnostic and prognostic biomarkers for colon cancer (12). Using miR expression patterns and target prediction, previous studies have observed that miR-185 expression is upregulated and results in loss of function of tumor suppressors in clear cell renal cell carcinoma (13) and lung squamous cell carcinoma (14).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-185 suppresses growth and invasion of colon cancer cells through inhibition of the hypoxia-inducible factor-2α pathway in vitro and in vivo

Tao

et al. 2014

Molecular Medicine Reports

View full text Add to dashboard Cite

Abstract. MicroRNAs (miRs) are small non-coding RNAs with regulatory roles, which are involved in a broad spectrum of physiological and pathological processes, including cancer development and progression. However, the function of miR-185 in the development of human colon cancer has not yet been investigated. In this study, the association between miR-185 expression and the clinicopathological characteristics of patients with colon cancer was analyzed using quantitative polymerase chain reaction (qPCR). Using a gain-of-function approach, the effects of miR-185 overexpression on the expression of hypoxia-inducible factor-2α (HIF-2α), proliferating cell nuclear antigen (PCNA) and matrix metallopeptidase-2 (MMP-2) were investigated in SW620 colon cancer cells using qPCR and western blotting. Functional analysis of cellular proliferative activities, by MTT assay, and invasive potential, by Transwell assay, was conducted on SW620 cells expressing low levels of miR-185. miR-185 was found to be significantly downregulated in cancer tissues compared with adjacent non-cancerous tissues, and was negatively correlated with lymph node metastasis of colon cancer (P<0.001). miR-185 overexpression in vitro impeded cellular proliferation and invasive potential with reduced expression of HIF-2α, PCNA and MMP-2 in SW620 cells transfected with an miR-185 mimic. In addition, the tumor volumes in SW620 subcutaneous nude mouse models treated with miR-185 were significantly smaller than those of the control group. In conclusion, these findings indicate that miR-185 as a tumor suppressor may affect the development of colon cancer cells via inhibition of HIF-2α signaling, suggesting that miR-185 may serve as a potential therapeutic target in cancer treatment.

show abstract

“…42,43 The miR-17-92 cluster is frequently over-expressed in a variety of tumors like B-cell lymphomas, breast, colon, lung, pancreas, prostate, and stomach cancers. 44,45 Some other tumorigenic miRNAs induced by Myc are miR-19a/b, implicated in cancer metabolism and cancer cell survival, 46 miR-18a which contributes to angiogenesis 47 and miR-9 which modulates the expression of mediators of metastasis. 48 Myc can also actively repress the transcription of numerous miRNAs, including some members of the let-7 and miR-29 families, as well as miR-15a/16-1, miR-26a and miR-34a.…”

Section: Mirnas As Cancer Modulatorsmentioning

confidence: 99%