MicroRNA-200b Stimulates Tumour Growth in TGFBR2-Null Colorectal Cancers by Negatively Regulating p27/kip1

Fu, Yuxuan; Li, Xianghua; Zhou, Ningtian; Du, Liqun; Sun, Yu; Zhang, Xiang; Ge, Yali

doi:10.1002/jcp.24497

Cited by 30 publications

(25 citation statements)

References 42 publications

(59 reference statements)

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“…Interestingly, the authors demonstrated increased SIX1 expression at the invasive border of clinical samples, which highlights the role that it may have in EMT modulation. 32 This interesting dichotomous role for the miR-200 family may be mediated by TGFBRII expression. While the miR-200 family is classically described in the ZEB1/E-cadherin pathway, there is an interesting differential expression noted between TGFBRII-expressive and deficient CRC cell lines.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

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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Section: Resultsmentioning

confidence: 99%

“…31 Conversely, TGF-b1 induces cellular proliferation in TGFBRII-deficient cell lines, with associated increased miR-200b. 32 This interesting dichotomous role for the miR-200 family may be mediated by TGFBRII expression. KRAS is a well described oncogene, which has been implicated in colorectal carcinogenesis.…”

Section: Other Pathwaysmentioning

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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“…Diminished numbers of iNKT cells in peripheral blood lymphocytes were found in persons with autoimmune diseases such as RA, systemic lupus erythematosus, systemic sclerosis, and Sjogren's syndrome (29). Therefore, miR-150 might (30). Tamoxifen inhibits miR-200 expression and promotes epithelial-to-mesenchymal transition by upregulating c-Myc in endometrial cancer cells (31).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

et al. 2014

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Periodontitis is a chronic inflammatory disease caused by specific bacteria and viruses. Local, systemic, and environmental factors affect the rate of disease progression. Immune responses to bacterial products, and the subsequent production of inflammatory cytokines, are crucial in the destruction of periodontal tissue. MicroRNAs (miRNAs) are a class of small RNAs that control various cell processes by negatively regulating protein-coding genes. In this study, we compared miRNA expression in inflamed and noninflamed gingival tissues from Japanese dental patients. Total RNAs were isolated from inflamed and noninflamed gingival tissues. miRNA expression profiles were examined by an miRNA microarray, and the data were analyzed by GeneSpring GX, Ingenuity Pathways Analysis, and the TargetScan databases. Observed miRNA expression levels in inflamed gingiva were confirmed by real-time PCR. The three most overexpressed (by >2.72-fold) miRNAs were hsa-miR-150, hsa-miR-223, and hsa-miR-200b, and the three most underexpressed (by <0.39-fold) miRNAs were hsa-miR-379, hsa-miR-199a-5p, and hsa-miR-214. In IPA analysis, hsa-miR-150, hsa-miR-223, and hsa-miR-200b were associated with inflammatory disease, organismal injury, abnormalities, urological disease, and cancer.

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“…As a consequence, cyclin D1, a downstream target of RND3, was increased along with S-phase entry (143). The association between miR-200b and RND3 could be extended to colorectal carcinoma (39) and human Tenon’s capsule fibroblasts (HTFs) (130). Using the informatics and qRT-PCR approach, Hurteau et al identified that Rnd3 may also be a target of miR-200c (58).…”

Section: Rnd3 Regulationmentioning

confidence: 99%

Pathophysiological Functions of Rnd 3/ RhoE

Jie

Andrade

Lin

et al. 2015

Comprehensive Physiology

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Rnd3, also known as RhoE, belongs to the Rnd subclass of the Rho family of small GTP-binding proteins. Rnd proteins are unique due to their inability to switch from a GTP-bound to GDP-bound conformation. Even though studies of the biological function of Rnd3 are far from being concluded, information is available regarding its expression pattern, cellular localization, and its activity, which can be altered depending on the conditions. The compiled data from these studies implies that Rnd3 may not be a traditional small GTPase. The basic role of Rnd3 is to report as an endogenous antagonist of RhoA signaling-mediated actin cytoskeleton dynamics, which specifically contributes to cell migration and neuron polarity. In addition, Rnd3 also plays a critical role in arresting cell cycle distribution, inhibiting cell growth, and inducing apoptosis and differentiation. Increasing data have shown that aberrant Rnd3 expression may be the leading cause of some systemic diseases; particularly highlighted in apoptotic cardiomyopathy, developmental arrhythmogenesis and heart failure, hydrocephalus, as well as tumor metastasis and chemotherapy resistance. Therefore, a better understanding of the function of Rnd3 under different physiological and pathological conditions, through the use of suitable models, would provide a novel insight into the origin and treatment of multiple human diseases.

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MicroRNA-200b Stimulates Tumour Growth in TGFBR2-Null Colorectal Cancers by Negatively Regulating p27/kip1

Cited by 30 publications

References 42 publications

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

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

MicroRNA expression in inflamed and noninflamed gingival tissues from Japanese patients

Pathophysiological Functions of Rnd 3/ RhoE

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