microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9

Wang, Feifei; Wang, Song; Xue, Wenhua; Cheng, Jingliang

doi:10.1007/s11010-016-2822-y

Cited by 31 publications

(16 citation statements)

References 25 publications

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“…We here corroborate previous reports demonstrating that ADAM9 promotes cancer cell migration (Nath et al, 2000;Wang et al, 2016;Zhou et al, 2001). The effect of ADAM9 on migration has been suggested to involve the interaction of ADAM9 with cell surface integrin adhesion receptors (Mazzocca et al, 2005).…”

Section: Discussionsupporting

confidence: 93%

“…1F,G). Thus, our findings support previous reports on the role of ADAM9 in integrin-mediated cell migration (Wang et al, 2016;Zhou et al, 2001).…”

Section: Introductionsupporting

confidence: 93%

“…As such, loss of ADAM9 results in the accumulation of integrin at the cell surface, which fails to properly support the actin cytoskeletal remodelling and coupled migratory behaviours commonly induced by integrin-mediated outside-in signalling (Legate et al, 2009). Cell migration is crucial for the invasion and metastatic spread of cancer cells (Hood and Cheresh, 2002), and while the reported effects of ADAM9 on cancer cell invasion are somewhat controversial (Fry and Toker, 2010;Mazzocca et al, 2005;Wang et al, 2016), it will be important to investigate the implication of ADAM9-mediated integrin regulation in this context.…”

Section: Discussionmentioning

confidence: 99%

“…Six different integrin subunits have been reported to interact with ADAM9, including α2β1, α3β1, α6β1, α9β1, α6β4 and αVβ5 (Karadag et al, 2006;Mazzocca et al, 2005;Nath et al, 2000;Zhou et al, 2001). While the exact function of these interactions is still unclear, they have been implicated in the adhesion and migration of several types of tumour cells (Cominetti et al, 2009;Josson et al, 2011;Martin et al, 2015;Mazzocca et al, 2005;Micocci et al, 2013;Wang et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

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Loss of ADAM9 expression impairs β1 integrin endocytosis, focal adhesion formation and cancer cell migration

Mygind

Schwarz

Sahgal

et al. 2018

Journal of Cell Science

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The transmembrane protease ADAM9 is frequently upregulated in human cancers, and it promotes tumour progression in mice. , ADAM9 regulates cancer cell adhesion and migration by interacting with integrins. However, how ADAM9 modulates integrin functions is not known. We here show that ADAM9 knockdown increases β1 integrin levels through mechanisms that are independent of its protease activity. In ADAM9-silenced cells, adhesion to collagen and fibronectin is reduced, suggesting an altered function of the accumulated integrins. Mechanistically, ADAM9 co-immunoprecipitates with β1 integrin, and both internalization and subsequent degradation of β1 integrin are significantly decreased in ADAM9-silenced cells, with no effect on β1 integrin recycling. Accordingly, the formation of focal adhesions and actin stress fibres in ADAM9-silenced cells is altered, possibly explaining the reduction in cell adhesion and migration in these cells. Taken together, our data provide mechanistic insight into the ADAM9-integrin interaction, demonstrating that ADAM9 regulates β1 integrin endocytosis. Moreover, our findings indicate that the reduced migration of ADAM9-silenced cells is, at least in part, caused by the accumulation and altered activity of β1 integrin at the cell surface.

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Section: Discussionsupporting

confidence: 93%

“…1F,G). Thus, our findings support previous reports on the role of ADAM9 in integrin-mediated cell migration (Wang et al, 2016;Zhou et al, 2001).…”

Section: Introductionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Loss of ADAM9 expression impairs β1 integrin endocytosis, focal adhesion formation and cancer cell migration

Mygind

Schwarz

Sahgal

et al. 2018

Journal of Cell Science

View full text Add to dashboard Cite

show abstract

“…For example, miR-590 inhibits the occurrence and metastasis of NSCLC via targeted regulation of ADAM9 gene expression (25). In addition, miR-146a acts as a tumor-suppressor gene by inhibiting the proliferation, invasion and metastasis of cervical cancer and colon cancer cells (26).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑138 inhibits SOX12 expression and the proliferation, invasion and migration of ovarian cancer cells

Zhu

Jin

2018

Exp Ther Med

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The aim of the present study was to investigate the expression and biological functions of microRNA (miR)-138 in ovarian cancer at the tissue and cellular levels, as well as its underlying mechanisms. A total of 47 patients with ovarian cancer were included in the present study. Ovarian cancer tissues were subjected to staging classification according to the FIGO 2000 criteria. Lymphatic metastasis was also examined. Ovarian cancer A2780 cells were transfected using liposomes. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression of miR-138. A Cell-Counting Kit 8 assay was used to examine cell viability, while a Transwell assay was employed to study cell invasion and migration. The effects of miR-138 on SOX12 protein expression were examined by western blot analysis. A dual luciferase reporter assay was performed to identify the direct interaction between miR-138 and SOX12 gene. Expression of miR-138 was downregulated in ovarian cancer tissues. The level of miR-138 in patients with ovarian cancer with lymphatic metastasis was significantly lower compared with patients without lymphatic metastasis. However, expression of miR-138 was not associated with the stage of ovarian cancer. Upregulation of miR-138 inhibited the proliferation and suppressed the invasion and migration of A2780 cells. SOX12 promoted the proliferation, invasion and migration of A2780 cells. In addition, miR-138 downregulated the expression of SOX12 via binding with the 3′-UTR of SOX12 gene. The present study demonstrates that miR-138 expression is downregulated in ovarian cancer tissues and miR-138 acts as a tumor suppressor gene by inhibiting SOX12 expression and the proliferation, invasion and migration of ovarian cancer cells.

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P65‐mediated miR‐590 inhibition modulates the chemoresistance of osteosarcoma to doxorubicin through targeting wild‐type p53‐induced phosphatase 1

Xiao

Lin

2018

J of Cellular Biochemistry

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Osteosarcoma (OS) is a primary malignant bone tumor with high morbidity. Developing new therapeutic approaches with neoadjuvant is of great interest in OS treatment. Reportedly, ataxia telangiectasia mutated (ATM)/ataxia telangiectasia and radiation resistance gene 3 related (ATR)‐p53 signaling is considered as a critical DNA damage signaling pathway sensitizing cancer cells to chemotherapies; while wild‐type p53‐induced phosphatase 1 (WIP1), an oncogene overexpressed in diverse cancers, has been regarded as a critical inhibitor in the ATM/ATR‐p53 DNA damage signaling pathway. Herein, the expression of WIP1 in OS tissues and cell lines was examined; to investigate the mechanism of WIP1 abnormal upregulation, online tools were used to predict the upstream regulatory microRNAs (miRNAs) targeting WIP1. Among the candidate miRNAs, the expression and detailed function of miR‐590 were validated. Through binding to the 3′‐untranslated region of WIP1, miR‐590 inhibited WIP1 expression and, therefore, enhanced the effect of Dox on OS cell proliferation and apoptosis through downstream ATM‐p53 signaling. Moreover, RELA could bind to the promoter region of miR‐590 to inhibit its expression, thereby affecting downstream WIP1 and ATM‐p53 signaling. The expression of p65 was upregulated in OS tissues, indicating that the effect of p65 inhibition on cell viability, apoptosis, and related mechanisms could be partially restored by miR‐590 inhibition. Taken together, these results showed that p65‐mediated miR‐590/WIP1/ATM‐p53 modulation might be a novel target to enhance the cellular effect of Dox on OS cell lines.

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microRNA-590 suppresses the tumorigenesis and invasiveness of non-small cell lung cancer cells by targeting ADAM9

Cited by 31 publications

References 25 publications

Loss of ADAM9 expression impairs β1 integrin endocytosis, focal adhesion formation and cancer cell migration

Loss of ADAM9 expression impairs β1 integrin endocytosis, focal adhesion formation and cancer cell migration

MicroRNA‑138 inhibits SOX12 expression and the proliferation, invasion and migration of ovarian cancer cells

P65‐mediated miR‐590 inhibition modulates the chemoresistance of osteosarcoma to doxorubicin through targeting wild‐type p53‐induced phosphatase 1

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