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

Mutlu, Merve; Raza, Umar; Saatçi, Özge; Eyüpoğlu, Erol; Yurdusev, Emre; Şahin, Özgür

doi:10.1007/s00109-016-1420-5

Cited by 114 publications

(99 citation statements)

References 143 publications

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“…In various cancers, miR-200c has been demonstrated to be an effective tumour suppressor that inhibits cancer development, proliferation, EMT, therapy resistance, and metastasis [17, 30]. Chang et al have shown that miR-200c inhibits EMT and metastasis of breast cancer cells by targeting HMGB1 [31], and Jiao et al have reported that miR-200c inhibits the metastasis of A549 cells by targeting ZEB2, an EMT regulator [32].…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies have demonstrated that endogenous miR-200c suppresses EMT by regulating cell adhesion through targeting the E-cadherin transcriptional repressors ZEB1 and ZEB2 [15, 16]. Furthermore, miR200c has also been reported to regulate proliferation, invasion, metastasis, and chemosensitivity in various cancers [17–19]. Nevertheless, it is not known whether miR-200c acts as a tumour suppressor through downregulating HMGB1 in NSCLC.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1

Liu

Chang

et al. 2017

PLoS ONE

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MicroRNAs (miRs) play critical roles in cancer development, proliferation, epithelial-mesenchymal transition (EMT), invasion, and migration through regulating the expression of oncogenes and tumour suppressor genes. Previous studies have indicated that miR-200c acts as a tumour suppressor in various cancers by downregulating high-mobility group box 1 (HMGB1) and thereby suppressing EMT and metastasis. In addition, miR-200c was reported to be downregulated and correlated with poor outcomes in non-small cell lung cancer (NSCLC). However, its functional role in HMGB1 regulation in NSCLC is still unclear. This study aimed to clarify whether miR-200c acts as a tumour suppressor in NSCLC by downregulating HMGB1, which is associated with EMT, invasion, cytoskeleton rearrangement, and migration in vitro and in vivo. In order to demonstrate HMGB1 downregulation by miR-200c, the NSCLC cell line A549 was transfected with miR-200c mimic or inhibitor. The mimic significantly reduced HMGB1 expression and suppressed EMT, invasion, and migration, while the inhibitor generated the opposite effects. Additionally, using xenograft mouse models, we confirmed that HMGB1 overexpression increased tumour EMT. In summary, our results demonstrated that miR-200c could suppress EMT, invasion, and migration of NSCLC cells by downregulating HMGB1.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1

Liu

Chang

et al. 2017

PLoS ONE

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“…miRNAs as a recent focus in tumor research serve an oncogenic or tumor-suppressive role in different cancer types via various pathways (17)(18)(19). miR-200c is a member of the miR-200 family, which is located on chromosome 12p13 and is closely associated with carcinogenesis and disease progression in a wide range of cancer types (20,21). To the best of our knowledge, there have been only 4 clinical studies on miR-200c expression in NSCLC to date, producing contradictory results (i.e.…”

Section: Discussionmentioning

confidence: 99%

Potential use of microRNA-200c as a prognostic marker in non-small cell lung cancer

Tian

Yue

et al. 2017

Oncology Letters

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Abstract. MicroRNAs (miRNAs/miRs) are a class of small, highly conserved non-coding RNAs that can serve either oncogenic or tumor-suppressive roles in a wide variety of tumors. miR-200c is a member of the miR-200 family whose specific role in non-small cell lung cancer (NSCLC) has not yet been elucidated. The purpose of the present study was to detect the expression level of miR-200c in NSCLC, and to analyze its association with clinicopathological factors and patient prognosis. The present study determined the expression levels of miR-200c in 110 tumor samples collected from patients diagnosed with NSCLC who underwent complete tumor resection with regional lymph node dissection, as assessed by reverse transcription-quantitative polymerase chain reaction. The association between the expression level of miR-200c and clinicopathological features and patient prognosis was also analyzed. The results showed that miR-200c overexpression was detected in 66 of the 110 cases and was significantly associated with positive lymph node metastasis (P<0.001). Univariate survival analysis demonstrated that high miR-200c expression, positive lymph node metastasis and advanced Tumor-Node-Metastasis (TNM) classification stage significantly predicted decreased 5-year disease-free survival rates (all P<0.05) and poor 5-year overall survival rates (all P<0.01), respectively. The results of multivariate Cox regression analysis showed that TNM stage and miR-200c expression retained its significance as an independent prognostic factor for unfavorable 5-year disease-free survival rates (P<0.05) and poor 5-year overall survival rates (P<0.01). The present findings suggest that miR-200c overexpression is significantly associated with poor survival rates in NSCLC and that miR-200c could play an oncogenic role. miR-200c may have clinical potential as a promising prognostic predictor for patients with NSCLC.

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“…In recent years, multiple miRNA-based drugs have been explored and have entered clinical testing [27,28] 31. Studies on this miRNA family revealed that it has versatile roles in cancer progression, drug resistance and oxidative stress [29,30].…”

Section: Introductionmentioning

confidence: 99%

miRNA-200c-3p is crucial in acute respiratory distress syndrome

et al. 2017

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Influenza infection and pneumonia are known to cause much of their mortality by inducing acute respiratory distress syndrome (ARDS), which is the most severe form of acute lung injury (ALI). Angiotensin-converting enzyme 2 (ACE2), which is a negative regulator of angiotensin II in the renin–angiotensin system, has been reported to have a crucial role in ALI. Downregulation of ACE2 is always associated with the ALI or ARDS induced by avian influenza virus, severe acute respiratory syndrome-coronavirus, respiratory syncytial virus and sepsis. However, the molecular mechanism of the decreased expression of ACE2 in ALI is unclear. Here we show that avian influenza virus H5N1 induced the upregulation of miR-200c-3p, which was then demonstrated to target the 3′-untranslated region of ACE2. Then, we found that nonstructural protein 1 and viral RNA of H5N1 contributed to the induction of miR-200c-3p during viral infection. Additionally, the synthetic analog of viral double-stranded RNA (poly (I:C)), bacterial lipopolysaccharide and lipoteichoic acid can all markedly increase the expression of miR-200c-3p in a nuclear factor-κB-dependent manner. Furthermore, markedly elevated plasma levels of miR-200c-3p were observed in severe pneumonia patients. The inhibition of miR-200c-3p ameliorated the ALI induced by H5N1 virus infection in vivo, indicating a potential therapeutic target. Therefore, we identify a shared mechanism of viral and bacterial lung infection-induced ALI/ARDS via nuclear factor-κB-dependent upregulation of miR-200c-3p to reduce ACE2 levels, which leads increased angiotensin II levels and subsequently causes lung injury.

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

Cited by 114 publications

References 143 publications

MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1

MicroRNA-200c inhibits epithelial-mesenchymal transition, invasion, and migration of lung cancer by targeting HMGB1

Potential use of microRNA-200c as a prognostic marker in non-small cell lung cancer

miRNA-200c-3p is crucial in acute respiratory distress syndrome

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