ADAM9 enhances CDCP1 by inhibiting miR-1 through EGFR signaling activation in lung cancer metastasis

Chiu, Kuo Liang; Lin, Yu; Kuo, Ting Ting; Lo, Chia Chien; Huang, Yu; Chang, Hsien Fang; Chuang, Eric Y.; Lin, Chia-Ho; Cheng, Wei‐Chung; Liu, Yen Nien; Lai, Liang‐Chuan; Sher, Yuh Pyng

doi:10.18632/oncotarget.17648

Cited by 28 publications

(23 citation statements)

References 39 publications

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“…Chiu showed that ADAM9 downregulated the miR-1 expression via activating the EGFR signaling pathways, which in turn enhanced CDCP1 expression to promote lung cancer progression. 31 Coincidentally, in our present study, we proposed a putative miR-1-3p binding on RMRP ( Figure 4A), which triggered us to ask whether RMRP-miR-1-3p could be a tumorrepressor axis in NSCLC samples. By dual-luciferase reporter assay, we found that miR-1-3p mimics suppressed the luciferase intensity of only RMRP-WT but not RMRP-MT ( Figure 4B), indicative of the specific binding of miR-1-3p with RMRP.…”

Section: Discussionsupporting

confidence: 49%

Long noncoding RNA RMRP promotes proliferation and invasion via targeting miR‐1‐3p in non–small‐cell lung cancer

Wang

Luo

Liu

et al. 2019

J of Cellular Biochemistry

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The long noncoding RNA component of mitochondrial RNA‐processing endoribonuclease (lncRNA RMRP) plays an important role in tumor development. In the present study, we determined the regulatory function of RMRP in non–small‐cell lung cancer (NSCLC). The NSCLC tissues and the adjacent nontumor tissues were collected for the study. The RMRP expression was detected by quantitative real time‐PCR in NSCLC and lung cancer cell lines. The functional validation experiments were performed to determine the role of RMRP on NSCLC progression. In addition, we identified the downstream target miRNAs for RMRP. The results showed that RMRP was elevated in NSCLC tissues and cell lines. High RMRP expression was closely associated with advanced stage for the clinical features and low overall survival in NSCLC patients. Functional assay showed that loss of RMRP markedly inhibited cell proliferation, migration, and invasion. Flow cytometry assay demonstrated that the inhibition of RMRP dramatically induced cell cycle arrest in the G0/G1 phase. Moreover, we found that the role of RMRP on NSCLC cell progression was modulated by the inhibition of miR‐1‐3p. Collectively, our results demonstrated that the “RMRP‐miR‐1‐3p” axis might promote NSCLC progression. Hence, these investigations will provide a therapeutic target and strategy for the treatment of NSCLC progression.

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Section: Discussionsupporting

confidence: 49%

Long noncoding RNA RMRP promotes proliferation and invasion via targeting miR‐1‐3p in non–small‐cell lung cancer

Wang

Luo

Liu

et al. 2019

J of Cellular Biochemistry

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“…This ADAM9-CDCP1 axis to lung cancer metastasis is also validated in several other reports as well [ 92 , 93 ]. The ADAM9-CDCP1 axis was confirmed to be necessary for lung cancer cell migration and survival in vitro and in vivo; and moreover, the authors demonstrated that ADAM9 decreases the expression of miR-1 and miR-218, which target the 3′-UTR of CDCP1 to suppress its expression.…”

Section: Role Of Adam9 In Cancerssupporting

confidence: 79%

An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases

Chou

Huang

Kuo

et al. 2020

IJMS

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ADAM9 (A disintegrin and a metalloprotease 9) is a membrane-anchored protein that participates in a variety of physiological functions, primarily through the disintegrin domain for adhesion and the metalloprotease domain for ectodomain shedding of a wide variety of cell surface proteins. ADAM9 influences the developmental process, inflammation, and degenerative diseases. Recently, increasing evidence has shown that ADAM9 plays an important role in tumor biology. Overexpression of ADAM9 has been found in several cancer types and is correlated with tumor aggressiveness and poor prognosis. In addition, through either proteolytic or non-proteolytic pathways, ADAM9 promotes tumor progression, therapeutic resistance, and metastasis of cancers. Therefore, comprehensively understanding the mechanism of ADAM9 is crucial for the development of therapeutic anti-cancer strategies. In this review, we summarize the current understanding of ADAM9 in biological function, pathophysiological diseases, and various cancers. Recent advances in therapeutic strategies using ADAM9-related pathways are presented as well.

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“…Many miRNAs have been reported down‐regulated in lung cancer, such as miR‐34b/c, miR‐1, miR‐206, miR‐145 and let 7 . Among them, miR‐1‐3p and miR‐206, which belong to muscle‐specific miRNAs and play key roles in skeletal muscle differentiation, have found exhibited inhibitory function in lung cancer growth, migration and invasion in recent years . However, other functions of these two miRNAs are not known.…”

Section: Discussionmentioning

confidence: 99%

miR‐1‐3p and miR‐206 sensitizes HGF‐induced gefitinib‐resistant human lung cancer cells through inhibition of c‐Met signalling and EMT

Jiao

Chen

Liu

et al. 2018

J Cellular Molecular Medi

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Hepatocyte growth factor (HGF) overexpression is an important mechanism in acquired epidermal growth factor receptor (EGFR) kinase inhibitor gefitinib resistance in lung cancers with EGFR activating mutations. MiR‐1‐3p and miR‐206 act as suppressors in lung cancer proliferation and metastasis. However, whether miR‐1‐3p and miR‐206 can overcome HGF‐induced gefitinib resistance in EGFR mutant lung cancer is not clear. In this study, we showed that miR‐1‐3p and miR‐206 restored the sensitivities of lung cancer cells PC‐9 and HCC‐827 to gefitinib in present of HGF. For the mechanisms, we demonstrated that both miR‐1‐3p and miR‐206 directly target HGF receptor c‐Met in lung cancer. Knockdown of c‐Met mimicked the effects of miR‐1‐3p and miR‐206 transfections Meanwhile, c‐Met overexpression attenuated the effects of miR‐1‐3p and miR‐206 in HGF‐induced gefitinib resistance of lung cancers. Furthermore, we showed that miR‐1‐3p and miR‐206 inhibited c‐Met downstream Akt and Erk pathway and blocked HGF‐induced epithelial‐mesenchymal transition (EMT). Finally, we demonstrated that miR‐1‐3p and miR‐206 can increase gefitinib sensitivity in xenograft mouse models in vivo. Our study for the first time indicated the new function of miR‐1‐3p and miR‐206 in overcoming HGF‐induced gefitinib resistance in EGFR mutant lung cancer cell.

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ADAM9 enhances CDCP1 by inhibiting miR-1 through EGFR signaling activation in lung cancer metastasis

Cited by 28 publications

References 39 publications

Long noncoding RNA RMRP promotes proliferation and invasion via targeting miR‐1‐3p in non–small‐cell lung cancer

Long noncoding RNA RMRP promotes proliferation and invasion via targeting miR‐1‐3p in non–small‐cell lung cancer

An Overview of ADAM9: Structure, Activation, and Regulation in Human Diseases

miR‐1‐3p and miR‐206 sensitizes HGF‐induced gefitinib‐resistant human lung cancer cells through inhibition of c‐Met signalling and EMT

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