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In the present study, the inhibitory effect of chlorogenic acid (CGA), a phenolic compound with potential antitumor effects, on circulating microRNA 31 (miR-31), was evaluated in RKO colon cancer cells. The capacity of gold nanoparticles (AuNPs) to enhance miR-31 quantification after treatment with CGA was assessed. RKO cells were treated with different concentrations of CGA for 24, 48 and 72 h, after which AuNPs coupled to CD81 were added to the supernatants. Total RNA was extracted, and miR-31 was quantified by reverse transcription-quantitative PCR. The results revealed an 85% decrease in miR-31 level following treatment with 1,000 µM CGA for 72 h, and the highest capacity to detect miR-31 (after treatment and isolation with AuNPs + CD81) was observed at 24 h. Furthermore, CGA decreased the expression of the miR-31 oncogene in an in vitro colon cancer model, and the use of AuNPs enhanced the levels of miRNA detection. The results suggest that miR-31 inhibition is one mechanism by which CGA decreases colon cancer cell proliferation. Moreover, AuNPs can increase the capacity of miR-31 quantification, representing a new strategy to develop non-invasive tools for the molecular diagnosis and monitoring of colon cancer.

The incidence of colorectal cancer (CRC) is increasing in young adults, but knowledge regarding the molecular features of sporadic early-onset colorectal cancer (SEOCRC) is limited. The objective of the present study was to investigate potential key tumorigenesis-associated genes and their regulatory microRNAs (miRNAs) in SEOCRC. Using miRNA and mRNA expression screening of SEOCRC and sporadic late-onset colorectal cancer (SLOCRC) by next generation sequencing (NGS) and bioinformatics, the SEOCRC-associated miRNAome and transcriptome were analyzed. In SEOCRC miRNA and mRNA expression profiles, the tumorigenesis-associated genes and their regulatory miRNAs were analyzed according to the miRTarBase database, and specific miRNA-mRNA pairs were selected as the candidate biomarkers in SEOCRC, which were further verified in another cohort of SEOCRC and SLOCRC patients' colon cancer and paracancerous tissues using reverse transcription-quantitative PCR and immunohistochemistry. Moreover, the clinical relevance of these paired signatures to clinicopathological features was determined in 80 patients with SEOCRC. The expression of dystrophin (DMD) was downregulated and that of miR-31-5p was upregulated in SEOCRC tissue compared with adjacent peritumoral tissue. While DMD and miR-31-5p were not differentially expressed in SLOCRC tissues compared with that in adjacent peritumoral tissues. The miR-31-5p-DMD axis was identified as the key regulatory axis specific to SEOCRC, and DMD expression was closely associated with TNM stage and lymph node metastasis. Importantly, Kaplan-Meier analysis revealed that patients with low DMD expression had significantly poorer overall survival, cancer specific survival and recurrence free survival compared with those with high expression of DMD. In conclusion, the miR-31-5p-DMD axis may serve as a novel biomarker in predicting the development of SEOCRC, and DMD can be used as a promising biomarker for the prognosis of SEOCRC.

Background We aimed to investigate whether MIR31 is an oncogene in human endometrial cancer and identify the target molecules associated with the malignant phenotype. Methods We investigated the growth potentials of MIR31-overexpressing HEC-50B cells in vitro and in vivo . In order to identify the target molecule of MIR31, a luciferase reporter assay was performed, and the corresponding downstream signaling pathway was examined using immunohistochemistry of human endometrial cancer tissues. We also investigated the MIR31 expression in 34 patients according to the postoperative risk of recurrence. Results The overexpression of MIR31 significantly promoted anchorage-independent growth in vitro and significantly increased the tumor forming potential in vivo . MIR31 significantly suppressed the luciferase activity of mRNA combined with the LATS2 3’-UTR and consequently promoted the translocation of YAP1, a key molecule in the Hippo pathway, into the nucleus. Meanwhile, the nuclear localization of YAP1 increased the transcription of CCND1. Furthermore, the expression levels of MIR31 were significantly increased (10.7-fold) in the patients (n = 27) with a high risk of recurrence compared to that observed in the low-risk patients (n = 7), and this higher expression correlated with a poor survival. Conclusions MIR31 functions as an oncogene in endometrial cancer by repressing the Hippo pathway. MIR31 is a potential new molecular marker for predicting the risk of recurrence and prognosis of endometrial cancer.

Background RNA‐binding protein Quaking‐5 (QKI‐5), a major isoform of QKIs, inhibits tumor progression in non‐small cell lung cancer (NSCLC). However, the underlying molecular mechanisms of QKI‐5 in the cell cycle of NSCLC are still largely unknown. Methods MTT, flow cytometry, and colony formation assays were used to investigate cellular phenotypic changes. Mice xenograft model was used to evaluate the antitumor activities of QKI‐5. Co‐immunoprecipitation, RNA immunoprecipitation (RIP), and RIP sequencing were used to investigate protein–protein interaction and protein–mRNA interaction. Results The QKI‐5 expression was downregulated in NSCLC tissues compared with that in paired normal adjacent lung tissues. Overexpression of QKI‐5 inhibited NSCLC cell proliferative and colony forming ability. In addition, QKI‐5 induced cell cycle arrest at G0/G1 phase through upregulating p21Waf1/Cip1 (p21) expression and downregulating cyclin D1, cyclin‐dependent kinase 4 (CDK4), and CDK6 expressions. Further analyses showed that QKI‐5 interacts with p21 protein and CDK4, CDK6 mRNAs, suggesting a critical function of QKI‐5 in cell cycle regulation. In agreement with in vitro study, the mouse xenograft models validated tumor suppressive functions of QKI‐5 in vivo through altering cell cycle G1‐phase‐associated proteins. Moreover, we demonstrated that QKI‐5 is a direct target of miR‐31. The QKI‐5 expression was anticorrelated with the miR‐31 expression in NSCLC patient samples. Conclusion Our results suggest that the miR‐31/QKI‐5/p21‐CDK4–CDK6 axis might have critical functions in the progression of NSCLC, and targeting this axis could serve as a potential therapeutic strategy for NSCLC. miR‐31 mediated QKI‐5 downregulation promoted tumor growth of NSCLC through regulating p21 protein and CDK4/6 mRNAs.