Effects of Decitabine on Invasion and Exosomal Expression of miR-200c and miR-141 in Oxaliplatin-Resistant Colorectal Cancer Cells

Tanaka, Shota; Hosokawa, Mika; Iwakawa, Seigo

doi:10.1248/bpb.b15-00129

Cited by 35 publications

(28 citation statements)

References 32 publications

(47 reference statements)

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“…A recent study, encompassing a panel of ovarian adenocarcinoma cell lines, has also shown the inhibitory action of miR-200c on TUBB3 expression, which also depends on the nuclear localization of an RNA-binding protein, HuR [56]. Another study revealed that decitabine treatmentdependent upregulation of miR-200c and miR-141 promotes epithelial-like characteristics in highly invasive oxaliplatinresistant colorectal cancer cells [57].…”

Section: Mir-200c and Chemotherapy Resistancementioning

confidence: 94%

miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance

et al. 2016

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MicroRNAs (miRNAs) are 20-22-nucleotide small endogenous non-coding RNAs which regulate gene expression at post-transcriptional level. In the last two decades, identification of almost 2600 miRNAs in human and their potential to be modulated opened a new avenue to target almost all hallmarks of cancer. miRNAs have been classified as tumor suppressors or oncogenes depending on the phenotype they induce, the targets they modulate, and the tissue where they function. miR-200c, an illustrious tumor suppressor, is one of the highly studied miRNAs in terms of development, stemness, proliferation, epithelial-mesenchymal transition (EMT), therapy resistance, and metastasis. In this review, we first focus on the regulation of miR-200c expression and its role in regulating EMT in a ZEB1/E-cadherin axis-dependent and ZEB1/E-cadherin axis-independent manner. We then describe the role of miR-200c in therapy resistance in terms of multidrug resistance, chemoresistance, targeted therapy resistance, and radiotherapy resistance in various cancer types. We highlight the importance of miR-200c at the intersection of EMT and chemoresistance. Furthermore, we show how miR-200c coordinates several important signaling cascades such as TGF-β signaling, PI3K/Akt signaling, Notch signaling, VEGF signaling, and NF-κB signaling. Finally, we discuss miR-200c as a potential prognostic/diagnostic biomarker in several diseases, but mainly focusing on cancer and its potential application in future therapeutics.

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Section: Mir-200c and Chemotherapy Resistancementioning

confidence: 94%

miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance

et al. 2016

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“…12,21 In oxaliplatin-resistant SW620 cells, which display mesenchymal features, treatment with a demethylating agent resulted in the restoration of expression of miR-200c and miR-141 as well as the epithelial marker, E-cadherin. 35,36 However, as previously mentioned, the demethylating agents used are not specific to the promoter regions of the miR-200 family, and other genes may be activated with demethylation and contribute to the phenotypic changes. It is hypothesized that repression of miR-200c and miR-141 was a marker for chemotherapy resistance.…”

Section: Therapeutic Potential: Mir-200 Family Changing Colon Cancer mentioning

confidence: 99%

The role of the miR‐200 family in epithelial–mesenchymal transition in colorectal cancer: a systematic review

O’Brien

Carter

Burton

et al. 2018

Intl Journal of Cancer

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Colorectal cancer (CRC) is associated with significant morbidity and mortality as many patients are diagnosed with advanced stage disease. MicroRNAs are small, noncoding RNA molecules that have a major role in gene expression regulation and are dysregulated in CRC. The miR-200 family is involved in epithelial-mesenchymal transition (EMT). This systematic review describes the roles of the miR-200 family in EMT in CRC. A search of electronic databases (PubMed and Embase) was conducted between January 2000 and July 2017. Both in vitro and human studies reporting on the miR-200 family and CRC were included. Studies describing molecular pathways and the role of the miR-200 family in the diagnostic and therapeutic management of CRC were analyzed. Thirty-four studies (22 in vitro and 18 human studies) were included. miR-200 family expression is regulated epigenetically and via transcriptional factor regulation. In vitro studies show that transfection of miR-200 family members into chemo-resistant colon cancer cell lines results in improved chemo-sensitivity and epithelial phenotype restoration. There is intra-tumoral variability in the tissue expression of miR-200 family members with decreased expression at the invasive front. Clinical studies in CRC patients have shown decreased primary tumor tissue expression of miR-429, miR-200a and miR-200c may be associated with worse survival. Conversely, increased blood levels of miR-141, miR-200a and miR-200c may be associated with worse outcomes. The miR-200 family has a central role in EMT. The miR200 family has potential for both prognostic and therapeutic management of CRC.

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“…2, 3 In addition, recent evidence has indicated that miRNAs can function as oncogenes or tumor suppressors. 4, 5 Many miRNAs were found to be aberrantly expressed in colorectal cancer (CRC) with the downregulation of miR-601, miR-192, miR-345, miR-215, and miR-612, and the upregulation of miR-223, miR-18a, miR-155, miR-31, and miR-224, when compared with those found in normal colon mucosa. 6, 7, 8, 9 Given their involvement in the initiation, progression, and metastasis of human cancers, some of these miRNAs have become studies of great interest.…”

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confidence: 99%

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

et al. 2016

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Altered expression of microRNA-590-5p (miR-590-5p) is involved in tumorigenesis, however, its role in colorectal cancer (CRC) remains to be determined. In this study, we focused on examining the effects of different expression levels of miR-590-5p in cancer cells and normal cells. Results showed that there are lower expression levels of miR-590-5p in human CRC cells and tissues than in normal control cells and tissues. Similarly, in our xenograft mouse model, knockdown of miR-590-5p promoted the progression of CRC. However, an overexpression of miR-590-5p in the mice inhibited angiogenesis, tumor growth, and lung metastasis. Nuclear factor 90 (NF90), a positive regulator of vascular endothelial growth factor (VEGF) mRNA stability and protein synthesis, was shown to be a direct target of miR-590-5p. The overexpression of NF90 restored VEGFA expression and rescued the loss of tumor angiogenesis caused by miR-590-5p. Conversely, the NF90-shRNA attenuated the increased tumor progression caused by the miR-590-5p inhibitor. Clinically, the levels of miR-590-5p were inversely correlated with those of NF90 and VEGFA in CRC tissues. Furthermore, knockdown of NF90 lead to a reduction of pri-miR-590 and an increase of mature miR-590-5p, suggesting a negative feedback loop between miR-590-5p and NF90. Collectively, these data establish miR-590-5p as an anti-onco-miR that inhibits CRC angiogenesis and metastasis through a new mechanism involving NF90/VEGFA signaling axis, highlighting the potential of miR-590-5p as a target for human CRC therapy.

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Effects of Decitabine on Invasion and Exosomal Expression of miR-200c and miR-141 in Oxaliplatin-Resistant Colorectal Cancer Cells

Cited by 35 publications

References 32 publications

miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance

miR-200c: a versatile watchdog in cancer progression, EMT, and drug resistance

The role of the miR‐200 family in epithelial–mesenchymal transition in colorectal cancer: a systematic review

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

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