Overexpression of miR‐199/214 is a distinctive feature of iron‐induced and asbestos‐induced sarcomatoid mesothelioma in rats

Okazaki, Yasumasa; Chew, Shan Hwu; Nagai, Hirotaka; Yamashita, Yoshihisa; Ohara, Hiroki; Jiang, Li; Akatsuka, Shinya; Takahashi, Takashi; Toyokuni, Shinya

doi:10.1111/cas.14405

Cited by 14 publications

(10 citation statements)

References 59 publications

(107 reference statements)

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“…it was also found that miR-214 significantly promoted the EMT process of melanoma, while cadM1 inhibited the eMT process. These results were similar to those of previous studies (46)(47)(48), thus indicating that mir-214 increased the invasion and migration of melanoma by downregulating cadM1 to promote the eMT process. However, it has also been revealed that mir-214 promotes cancer progression by activating the nF-κB signaling pathway (49).…”

Section: Discussionsupporting

confidence: 92%

MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

Wang

Wen

et al. 2020

Mol Med Rep

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Melanoma is a malignant skin cancer type associated with a high mortality rate, but its treatment is currently not ideal. Both microrna (mir)-214 and cell adhesion molecule 1 (cadM1) are differentially expressed in melanoma, but their role in this cancer type remains unknown. Therefore, the aim of the present study was to investigate the role of cadM1 and mir-214 in melanoma to identify novel targets for its treatment. The expression levels of cadM1 and mir-214 in cells were detected by reverse transcription-quantitative Pcr (rT-qPcr). Moreover, cell viability, migration and invasion were measured by MTT, wound healing and Transwell assays, respectively. in addition, the relative expression levels of epithelial-mesenchymal transition (eMT)-related proteins in cells were detected by rT-qPcr and western blotting. it was found that the expression of cadM1 was inhibited in melanoma cells, while mir-214 expression was increased during melanoma tumorigenesis. Furthermore, mir-214 mimics promoted the viability, migration and invasion of melanoma cells. it was also demonstrated that the downregulation of cadM1 reversed the inhibitory effect of the mir-214 inhibitor in melanoma. Moreover, overexpression of cadM1 inhibited the eMT process in melanoma, while the mir-214 inhibitor suppressed the eMT process. The results also indicated that mir-214 promoted the eMT process by downregulating cadM1, which may represent a novel mechanism for the progression of melanoma.

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Section: Discussionsupporting

confidence: 92%

MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

Wang

Wen

et al. 2020

Mol Med Rep

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“…30 The association of miRNA expression with lung cancer has not well been investigated in experimental animals, although a recent study has shown that miR-199 and miR-214 are overexpressed in asbestos-induced sarcomatoid mesothelioma of rats. 13 A recent epidemiological study has reported that serum miR-126 and miR-222 expression is increased in patients with asbestos-induced non-small cell lung cancer compared with disease-free subjects. 31 This is the first study showing that miR-21 was upregulated and its potential target genes PDCD4 and RECK were downregulated in lung tissues of asbestosexposed animals, raising a possibility that these molecules participate in asbestos-induced lung carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…[10][11][12] A recent animal study has demonstrated that several miRNAs are overexpressed in asbestos-induced rat sarcomatoid mesothelioma. 13 However, the role of miRNA in the pathogenesis of asbestos-induced carcinogenesis is not well understood. In addition, the expression pattern of miRNA and predicted target genes has not been investigated in lung tissues of asbestos-exposed animals.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA expression in lung tissues of asbestos-exposed mice: Upregulation of miR-21 and downregulation of tumor suppressor genes Pdcd4 and Reck

Hiraku

Watanabe

Kaneko

et al. 2021

Journal of Occupational Health

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Objectives: Asbestos causes lung cancer and malignant mesothelioma in humans, but the precise mechanism has not been well understood. MicroRNA (miRNA) is a short non-coding RNA that suppresses gene expression and participates in human diseases including cancer. In this study, we examined the expression levels of miRNA and potential target genes in lung tissues of asbestosexposed mice by microarray analysis. Methods:We intratracheally administered asbestos (chrysotile and crocidolite, 0.05 or 0.2 mg/instillation) to 6-week-old ICR male mice four times weekly. We extracted total RNA from lung tissues and performed microarray analysis for miRNA and gene expression. We also carried out real-time polymerase chain reaction (PCR), Western blotting, and immunohistochemistry to confirm the results of microarray analysis.Results: Microarray analysis revealed that the expression levels of 14 miRNAs were significantly changed by chrysotile and/or crocidolite (>2-fold, P < .05).Especially, miR-21, an oncogenic miRNA, was significantly upregulated by both chrysotile and crocidolite. In database analysis, miR-21 was predicted to target tumor suppressor genes programmed cell death 4 (Pdcd4) and reversioninducing-cysteine-rich protein with kazal motifs (Reck). Although real-time PCR showed that Pdcd4 was not significantly downregulated by asbestos exposure, Western blotting and immunohistochemistry revealed that PDCD4 expression was reduced especially by chrysotile. Reck was significantly downregulated by chrysotile in real-time PCR and immunohistochemistry.Conclusions: This is the first study demonstrating that miR-21 was upregulated and corresponding tumor suppressor genes were downregulated in lung tissues of asbestos-exposed animals. These molecular events are considered to be an early response to asbestos exposure and may contribute to pulmonary toxicity and carcinogenesis.

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“…A prognostic value has even been associated with EMT markers in malignant mesotheliomas [20] and in metastatic lung adenocarcinomas [36]. To underline the crucial role of Twist in the EMT-associated aggressiveness of the MPM, the association between the presence of Twist in MPM and a poor prognosis was highlighted [37]. Moreover, it has been shown that ZEB-1 and Twist are also overexpressed in mesothelioma and primary lung adenocarcinomas, and in the latter, SNAIL-1 overexpression has been associated with a poor survival rate [36].…”

Section: Emt In Mpm Development and Metastasismentioning

confidence: 99%

The Epithelial-to-Mesenchymal Transition (EMT) in the Development and Metastasis of Malignant Pleural Mesothelioma

Ramundo

Zanirato

Aldieri

2021

IJMS

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Malignant pleural mesothelioma (MPM) is an aggressive tumor mainly associated with asbestos exposure and is characterized by a very difficult pharmacological approach. One of the molecular mechanisms associated with cancer onset and invasiveness is the epithelial-to-mesenchymal transition (EMT), an event induced by different types of inducers, such as transforming growth factor β (TGFβ), the main inducer of EMT, and oxidative stress. MPM development and metastasis have been correlated to EMT; On one hand, EMT mediates the effects exerted by asbestos fibers in the mesothelium, particularly via increased oxidative stress and TGFβ levels evoked by asbestos exposure, thus promoting a malignant phenotype, and on the other hand, MPM acquires invasiveness via the EMT event, as shown by an upregulation of mesenchymal markers or, although indirectly, some miRNAs or non-coding RNAs, all demonstrated to be involved in cancer onset and metastasis. This review aims to better describe how EMT is involved in driving the development and invasiveness of MPM, in an attempt to open new scenarios that are useful in the identification of predictive markers and to improve the pharmacological approach against this aggressive cancer.

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Overexpression of miR‐199/214 is a distinctive feature of iron‐induced and asbestos‐induced sarcomatoid mesothelioma in rats

Cited by 14 publications

References 59 publications

MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

MicroRNA‑214 promotes the EMT process in melanoma by downregulating CADM1 expression

MicroRNA expression in lung tissues of asbestos-exposed mice: Upregulation of miR-21 and downregulation of tumor suppressor genes Pdcd4 and Reck

The Epithelial-to-Mesenchymal Transition (EMT) in the Development and Metastasis of Malignant Pleural Mesothelioma

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