microRNA-203 suppresses invasion and epithelial-mesenchymal transition induction via targeting NUAK1 in head and neck cancer

Obayashi, Mariko; Yoshida, Maki; Takemoto, Tsunematsu; Ogawa, Ikuko; Sasahira, Tomonori; Kuniyasu, Hiroki; Imoto, Issei; Abiko, Yoshimitsu; Xu, Dan; Fukunaga, Saori; Tahara, Hidetoshi; Kudo, Yasusei; Nagao, Toshitaka; Takata, Takashi

doi:10.18632/oncotarget.6972

Cited by 66 publications

(51 citation statements)

References 50 publications

(58 reference statements)

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“…miR‐203 is another microRNA frequently deregulated in different types of cancer (Li, Gao, & Zhang, ; Tang et al., ; Tian et al., ; Zhao et al., ). Focusing on this specific miRNA, our findings are corroborating previous studies reporting a tumor suppressor role of miR‐203 in HNSCC, as miR‐203 expression was significantly downregulated in patients with lymph node metastasis (Benaich et al., ; Obayashi et al., ). These studies showed that miR‐203 inhibited HNSCC invasion and epithelial–mesenchymal transition by targeting a network of prometastatic proteins, including LASP1, SPARC, and NUAK1 (Benaich et al., ; Obayashi et al., ).…”

Section: Discussionsupporting

confidence: 90%

“…Focusing on this specific miRNA, our findings are corroborating previous studies reporting a tumor suppressor role of miR‐203 in HNSCC, as miR‐203 expression was significantly downregulated in patients with lymph node metastasis (Benaich et al., ; Obayashi et al., ). These studies showed that miR‐203 inhibited HNSCC invasion and epithelial–mesenchymal transition by targeting a network of prometastatic proteins, including LASP1, SPARC, and NUAK1 (Benaich et al., ; Obayashi et al., ). Altogether, our results reinforce the hypothesis that miR‐203 may be a potential new diagnostic and therapeutic target for the treatment of HNSCC.…”

Section: Discussionsupporting

confidence: 90%

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Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

et al. 2018

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 90%

Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

et al. 2018

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“…Up to recent years, it has become increasingly apparent that miRNAs are critical regulators of a wide variety of biological processes, including EMT and tumorigenesis. It has been reported that miR-10b and miR-203 can promote or suppress cancer metastasis and invasion by modulating EMT [27,28]. The present study revealed that mesenchymal markers, such as N-cadherin and vimentin, were down-regulated, but epithelial cell markers, such as E-cadherin were up-regulated in PCa cells overexpressing miR-802 , indicating that miR-802 suppresses EMT.…”

Section: Discussionsupporting

confidence: 51%

microRNA-802 inhibits epithelial-mesenchymal transition through targeting flotillin-2 in human prostate cancer

Wang

Shao

2017

Bioscience Reports

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miRNAs are a class of non-coding RNAs that exert critical roles in various biological processes. The aim of the present study was to identify the functional roles of miR-802 in regulating epithelial–mesenchymal transition (EMT) in prostate cancer (PCa). miR-802 expression was detected in 73 pairs of PCa samples and PCa cell lines (PC3 and DU145 cells) by qRT-PCR. Cell proliferation was detected using MTT assay, and cell apoptosis was evaluated using flow cytometry. Transwell assay was conducted to investigate cell migration and invasion. Expression analysis of a set of EMT markers was performed to explore whether miR-802 is involved in EMT program. Xenograft model was established to investigate the function of miR-802 in carcinogenesis in vivo. The direct regulation of Flotillin-2 (Flot2) by miR-802 was identified using luciferase reporter assay. miR-802 was remarkably down-regulated in PCa tissues and cell lines. Gain-of-function trails showed that miR-802 serves as an ‘oncosuppressor’ in PCa through inhibiting cell proliferation and promoting cell apoptosis in vitro. Overexpression of miR-802 significantly suppressed in vivo PCa tumor growth. Luciferase reporter analysis identified Flot2 as a direct target of miR-802 in PCa cells. Overexpressed miR-802 significantly suppressed EMT, migration and invasion in PCa cells by regulating Flot2. We identified miR-802 as a novel tumor suppressor in PCa progression and elucidated a novel mechanism of the miR-802/Flot2 axis in the regulation of EMT, which may be a potential therapeutic target.

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“…As already reported, ARK5, as a downstream substrate of Akt, was directly activated by phosphorylation at its Ser 600 , and therefore resulting in stimulation of cancer cells invasion and metastasis [15]. To date, ARK5 has been confirmed to facilitate cancer metastasis through the induction of EMT or the activation of matrix metalloproteinase 2 (MMP2) and MMP9 in certain human malignancies [20, 26-28]. However, few investigations about the effect of ARK5 on the GC invasion and metastasis have been reported.…”

Section: Discussionmentioning

confidence: 93%

Knockdown of ARK5 Expression Suppresses Invasion and Metastasis of Gastric Cancer

Chen¹,

Liu²,

Xu³

et al. 2017

Cell Physiol Biochem

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Background/Aims: Gastric cancer (GC) is a common and lethal malignancy, and AMP-activated protein kinase-related kinase 5 (ARK5) has been discovered to promote cancer metastasis in certain types of cancer. In this study, we explored the role of ARK5 in GC invasion and metastasis. Methods: ARK5 and epithelial-mesenchymal transition (EMT)-related markers were determined by immunohistochemistry and western blot in GC specimens. Other methods including stably transfected against ARK5 into SGC7901 and AGS cells, western blot, migration and invasion assays in vitro and nude mice tumorigenicity in vivo were also employed. Results: The results demonstrated that ARK5 expression was increased and positively correlated with metastasis, EMT-related markers and poor prognosis in patients with GC. Knockdown of ARK5 expression remarkably suppressed GC cells invasion and metastasis via regulating EMT, rather than proliferation in vitro and in vivo. And knockdown of ARK5 expression in GC cells resulted in the down-regulation of the mTOR/p70S6k signals, Slug and SIP1. Conclusion: The elevated ARK5 expression was closely associated with cancer metastasis and patient survival, and it seemed to function in GC cells migration and invasion via EMT alteration, together with the alteration of the mTOR/p70S6k signals, Slug and SIP1, thus providing a potential therapeutic target for GC.

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microRNA-203 suppresses invasion and epithelial-mesenchymal transition induction via targeting NUAK1 in head and neck cancer

Cited by 66 publications

References 50 publications

Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

Clinicopathological significance of miR‐26, miR‐107, miR‐125b, and miR‐203 in head and neck carcinomas

microRNA-802 inhibits epithelial-mesenchymal transition through targeting flotillin-2 in human prostate cancer

Knockdown of ARK5 Expression Suppresses Invasion and Metastasis of Gastric Cancer

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