Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer

Wang, J; Tian, Xin; Han, Renfang; Zhang, X; Wang, X; Shen, Haitao; Li, Xue; Liu, Y; Yan, Xixin; Shen, Jun; Mannoor, Kaiissar; Deepak, Janaki; Donahue, James M.; Stass, Sanford A.; Xing, Lingxiao; Jiang, Feng

doi:10.1038/onc.2013.42

Cited by 205 publications

(218 citation statements)

References 31 publications

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“…In addition, miR-216b, miR-186, miR-337-3p and miR-760 were found to cooperatively promote cellular senescence through the p53-p21 (Cip1/ WAF1) pathway in human colorectal cancer cells (75). Given that the overexpression of miR-486-5p is closely correlated with the downregulated expression of ARHGAP5 in lung tumor tissues, which considerably inhibits lung cancer cell migration and invasion, miR-486-5p may act as a tumor suppressor contributing to the progression and metastasis of non-small cell lung cancer (76). Actually, the biological processes including cell proliferation, invasion, growth and metastasis in which miR-216b and miR-486-5p are involved are closely related to the development of drug resistance in cancers (49,77), and the annotation of biological processes also suggests that cell proliferation and growth are associated with drug resistance.…”

Section: Microrna-mrna Prediction Tool ------------------------------mentioning

confidence: 99%

Upregulation of NEK2 is associated with drug resistance in ovarian cancer

et al. 2013

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Abstract. NEK2 [NIMA (never in mitosis gene A)-related expressed kinase 2] is associated with various biological behaviors in the development of cancer, while research concerning its association with drug resistance is limited. The association of NEK2 with drug resistance in ovarian cancer has not yet been reported. In the present study, on the basis of microarray results from Oncomine and the GEO Profiles online database, we revealed that NEK2 mRNA expression in ovarian cancer tissues is upregulated. In addition, its expression in drugresistant ovarian cancer cells was upregulated when compared with expression with their sensitive or parental counterparts. Finally, we performed a comprehensive bioinformatic analysis consisting of protein/gene-protein/gene interaction network, annotation of biological processes and microRNA-mRNA interaction analysis. We observed that NEK2 directly or indirectly interacts with a number of genes, proteins, microRNAs and biological processes associated with drug resistance in ovarian and other types of cancer. These results indicate that NEK2 contributes to drug resistance in ovarian cancer and it may be an important therapeutic target.

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Section: Microrna-mrna Prediction Tool ------------------------------mentioning

confidence: 99%

Upregulation of NEK2 is associated with drug resistance in ovarian cancer

et al. 2013

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“…Previous studies demonstrated the importance of miRNAs during the development, classification, diagnosis and prognosis of CRC (7)(8)(9). miR-486-5p has been reported to function as a tumor suppressor in various types of cancer, including non-small-cell lung (10) and primary gastric cancer (11).…”

Section: Introductionmentioning

confidence: 99%

miR-486-5p regulates the migration and invasion of colorectal cancer cells through targeting PIK3R1

Zhang

Fu²,

Zhang³

et al. 2018

Oncol Lett

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Abstract. The aim of the present study was to investigate the function of microRNA (miR)-486-5p in colorectal cancer (CRC). Tumor and adjacent normal mucosal tissue samples were collected from patients with CRC. Differences in the expression levels of miR-486-5p between tumor tissues and adjacent normal mucosal tissues were examined using reverse transcription-quantitative polymerase chain reaction. The results demonstrated that miR-486-5p was significantly decreased in tumor tissues compared with the adjacent normal mucosal tissues. Additionally, in vitro experiments were conducted using SW620 CRC cells. The effects of miR-486-5p mimics on cell invasion and cell migration were evaluated using a Transwell assay and a wound-healing assay, respectively. The results demonstrated that treatment with miR-486-5p mimics decreased the migratory and invasive ability of the cells compared with that in the blank and NC control groups, although the underlying molecular mechanisms were not determined. Protein expression levels of phosphatidylinositol 3-kinase regulatory subunit 1 (PIK3R1), matrix metallopeptidases-2 and -9, and phosphorylated (p)-AKT were examined using western blot analysis. The results demonstrated that the expression levels of these proteins decreased in response to treatment with miR-486-5p mimics in comparison with the blank and NC control groups. Taken together, the findings of the present study indicated that miR-486-5p mimics inhibited the progression of CRC by inhibiting the activation of AKT signaling pathway via targeting PIK3R1. Therefore, miR-486-5p may be a potential target for CRC treatment.

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“…In addition, miR-451 is involved in mediating the resistance of breast cancer cells to the chemotherapeutic drug doxorubicin through regulating MDR1 expression (21). Aberrant expression of miR-486-5p is a frequent molecular event that has important functions in human malignances (22,23); however, evidence of biological roles for miR-451 and miR-486 in relapsed/refractory AML has not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

miR-181b increases drug sensitivity in acute myeloid leukemia via targeting HMGB1 and Mcl-1

Zhang

et al. 2014

International Journal of Oncology

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Abstract. Multidrug resistance (MDR) remains the major cause of disease relapse and poor prognosis in adults with acute myeloid leukemia (AML). Emerging evidence shows that drug resistance not only exists against conventional chemotherapeutic drugs, but also limits the efficacy of new biological agents. Therefore, it is important to elucidate the mechanisms through which AML patients develop drug resistance. MicroRNAs have been shown to play an important role in regulating the chemotherapy resistance in AML. A detailed understanding of the mechanisms of microRNA that are clinically relevant in AML may enhance our ability to predict and overcome drug resistance. Here, we demonstrated, for the first time, that miR-181b was decreased significantly in human multidrug-resistant leukemia cells and relapsed/refractory AML patient samples. Overexpression of miR-181b increased the sensitivity of leukemia cells to cytotoxic chemotherapeutic agents and promoted drug-induced apoptosis. Moreover, miR-181b inhibited HMGB1 and Mcl-1 expression by direct binding to their 3'-untranslated regions. In addition, HMGB1 was expressed at high levels in relapsed/refractory AML patients and suppression of HMGB1 via RNA interference sensitized multidrug-resistant leukemia cells to chemotherapy and induced apoptosis. In conclusion, these results provide a strong rationale for the development of miR-181b-based therapeutic strategies for the enhancement of efficacy in AML treatment.

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Downregulation of miR-486-5p contributes to tumor progression and metastasis by targeting protumorigenic ARHGAP5 in lung cancer

Cited by 205 publications

References 31 publications

Upregulation of NEK2 is associated with drug resistance in ovarian cancer

Upregulation of NEK2 is associated with drug resistance in ovarian cancer

miR-486-5p regulates the migration and invasion of colorectal cancer cells through targeting PIK3R1

miR-181b increases drug sensitivity in acute myeloid leukemia via targeting HMGB1 and Mcl-1

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