MicroRNA 211 expression is upregulated and associated with poor prognosis in colorectal cancer: a case–control study

Abstract

Increasingly more evidence support the role of the microRNAs (miRNA) in tumorigenesis. The role of up/downregulation microRNA-211 (miR-211) during human tumorigenesis is still contentious and may exhibit tissue-specific regulatory manner, but the exhaustive mechanisms underlying its pro/anti-oncogenic effects remain to be unknown. Sixty-six patients that were diagnosed and operated with colorectal cancer (CRC) and sixty-five healthy cases that were age and sex compatible with them were included in our study. miRNA was isolated from the formalin-fixed paraffin-embedded (FFPE) tissues of all cases. The expression level of miR-211 in matched normal and tumor tissues of CRC group and healthy group was evaluated using a quantitative real-time RT-PCR (qRT-PCR). Based on the average miR-211 levels, two groups of low or high expression were formed in CRC group. Correlation of the patients' clinicopathological factors and survival was also analyzed. No statistically significant differences were found in miR-211 levels among tumorous and normal tissues of CRC patient group (P = 0.59). Also, no statistically significant correlation was determined between clinicopathological factors and miR-211 expression level in CRC group. However, miR-211 expression levels between the CRC group and the healthy group were determined to be of statistical significance (P < 0.0001). There were 33 (50 %) CRC patients that expressed low levels of miR-211 and 33 (50 %) CRC patients that expressed high levels of miR-211. A median survival between low levels of miR-211 group and high levels of miR-211 group was evaluated via Kaplan-Meier, and the difference was of statistical significance (P = 0.035). The univariate analysis of the factors that may affect survival indicated invasion depth (P = 0.063), lymphovascular invasion (P = 0.011), perineural invasion (P = 0.009), and miR-211 expression level (P = 0.041) presence to be effective. In the multivariate analysis of these factors with overall survival, only miR-211 expression level (P = 0.01) was effective on overall survival. Our results suggest for the first time that miR-211 expressed more in CRC patients than in healthy group could be a new prognostic biomarker in order to predict survival. Independent studies are needed to validate our findings in a larger series, as well as in cancer of different tissues.

RETRACTED: The Effect of MCM3AP-AS1/miR-211/KLF5/AGGF1 Axis Regulating Glioblastoma Angiogenesis

“…miR-211 is located in intron 6 of the TRPM1 gene on chromosome 15 ( Margue et al, 2013 ). A recent publication has shown that miR-211 exerts tumor suppressive function in colorectal cancer through inhibiting the proliferation, migration, and invasion of colorectal cancer cells ( Sumbul et al, 2015 ). Moreover, it has been reported that expression of miR-211 is downregulated in glioma tissues.…”

Tumor suppressor miR-211-5p is associated with cellular migration, proliferation and apoptosis in renal cell carcinoma

“…However, a study by Xu et al (23) revealed that miR-211-3p served as an oncogene in CRC and promoted cell proliferation by targeting lncRNA tumor suppressor candidate 7 in CRC cell lines. Furthermore, a case-control study discovered that miR-211 was associated with poor prognosis in CRC, while no statistically significant differences between clinicopathological factors and miR-211 expression level were identified in the CRC group (24).…”

NF-κB-Induced MicroRNA-211 Inhibits Interleukin-10 in Macrophages of Rats with Lipopolysaccharide-Induced Acute Respiratory Distress Syndrome

“…For example, Mazar et al demonstrated that miR-211 functioned as a metabolic switch in human melanoma cells [24]. In a case-control study, Sumbul et al reported that miR-211 was up-regulated and associated with the poor prognosis in colorectal cancers [25]. MiR-211 has also been suggested as a tumor suppressor miRNA via inhibiting cell proliferation and invasion of gastric cancer by down-regulating SOX4 [26].…”