A novel inhibitor of <scp>ADAM</scp>17 sensitizes colorectal cancer cells to 5‐Fluorouracil by reversing Notch and epithelial‐mesenchymal transition in vitro and in vivo

Li, Dandan; Zhao, Chang-Hao; Ding, Huaiwei; Wu, Qiong; Ren, Tianshu; Wang, Jian; Chen, Congqin; Zhao, Qingchun

doi:10.1111/cpr.12480

Cited by 49 publications

(37 citation statements)

References 57 publications

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“…To our knowledge, this study is the first report that ADAM9 overexpression promotes the cell proliferation, migration, and invasion in TNBC cells by activating the AKT/NF-κB pathway. ADAM9 expression was increased in tumor tissues from TNBC patients and TNBC cells compared with the non-TNBC tumor tissues and cell lines, which is consistent with the previous finding that ADAM9 was overexpressed and associated with a more aggressive phenotype of breast cancer (26). Interestingly, MCF-10A (a normal epithelial breast cell line) expresses relatively high ADAM9 expression than non-TNBC cell lines, which might be caused by the culture method of immortalized MCF-10A cell line.…”

Section: Discussionsupporting

confidence: 90%

“…Besides, several members of ADAMs were reported to involve in epithelial-mesenchymal transition (EMT) processes in cancer. ADAM12 is participated in TGF-β mediated EMT in breast cancer, while ADAM17 induces EMT in colorectal cancer via Notch signaling pathway (25,26). In this study, we found that ADAM9 expression is upregulated in TNBC cells and patients compared with the non-TNBC.…”

Section: Discussionmentioning

confidence: 48%

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ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-κB Pathway

Zhou

Cho

et al. 2020

Front. Med.

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Upregulation of a disintegrin and metalloprotease 9 (ADAM9) is correlated with progression of cancers, such as prostate, bladder, and pancreatic cancers. However, its role in triple-negative breast cancer (TNBC) is still unclear. Our study aimed to investigate whether ADAM9 is upregulated and promoted the aggressiveness in TNBC. Breast cancer cell lines and patient specimens were used to evaluate the ADAM9 expression by western blotting and immunohistochemistry staining, respectively. Compared with the non-TNBC, ADAM9 expression was significantly increased in TNBC cells and TNBC patient specimens. Based on the data acquired from public databases, the correlation between ADAM9 expression and breast cancer patient survival was analyzed by Kaplan-Meier method. It was shown that ADAM9 overexpression was significantly correlated with poorer survival in patients with TNBC. Furthermore, ADAM9 in TNBC cells was knocked down by small interference RNA and then studied by the MTT/colony formation assay, wound healing assay and transwell invasion assay on the cell proliferation, migration, and invasion, respectively. We found that inhibiting ADAM9 expression suppressed TNBC cell proliferation, migration, and invasion by lowering the activation of AKT/NF-κB pathway. Our results demonstrated that ADAM9 is an important molecule in mediating TNBC aggressiveness and may be a potential useful therapeutic target in TNBC treatment.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 48%

ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-κB Pathway

Zhou

Cho

et al. 2020

Front. Med.

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“…Downregulation of the activity of the Notch signaling pathway by various pathways can reduce the resistance of cells to various damaging factors. This increases the sensitivity of cells to molecular targeted drugs and offers safer and more effective treatments (i.e., cytotoxic chemotherapy drugs and radiation therapy) [64][65][66][67] .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents

et al. 2019

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Molecular targeted agents, such as sorafenib, remain the only choice of an antitumor drug for the treatment of advanced hepatocellular carcinoma (HCC). The Notch signaling pathway plays central roles in regulating the cellular injury/stress response, anti-apoptosis, or epithelial-mesenchymal transition process in HCC cells, and is a promising target for enhancing the sensitivity of HCC cells to antitumor agents. The ADAM metalloprotease domain-17 (ADAM-17) mediates the cleavage and activation of Notch protein. In the present study, microRNA-3163 (miR-3163), which binds to the 3′-untranslated region of ADAM-17, was screened using online methods. miRDB and pre-miR-3163 sequences were prepared into lentivirus particles to infect HCC cells. miR-3163 targeted ADAM-17 and inhibited the activation of the Notch signaling pathway. Infection of HCC cells with miR-3163 enhanced their sensitivity to molecular targeted agents, such as sorafenib. Therefore, miR-3163 may contribute to the development of more effective strategies for the treatment of advanced HCC.

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“…pathway (Li et al, 2018), and induces metastasis in gastric cancer through activation of Notch and Wnt signaling pathways (Li et al, 2019c). A review article discussed ADAM17 inhibitors for inflammation and cancer therapy (Kanda et al, 2017).…”

Section: Analysis Of Genetic Alterations Of the Pbmentioning

confidence: 99%

Integrative Bioinformatics Analysis Reveals Potential Target Genes and TNFα Signaling Inhibition by Brazilin in Metastatic Breast Cancer Cells

Hermawan

Putri

2020

Asian Pac J Cancer Prev

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A novel inhibitor of ADAM17 sensitizes colorectal cancer cells to 5‐Fluorouracil by reversing Notch and epithelial‐mesenchymal transition in vitro and in vivo

Abstract: A novel ADAM17 inhibitor ZLDI-8 may be a potential chemosensitizer which sensitized CRC cells to 5-fluorouracil or irinotecan by reversing Notch and EMT pathways.

Cited by 49 publications

References 57 publications

ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-κB Pathway

ADAM9 Mediates Triple-Negative Breast Cancer Progression via AKT/NF-κB Pathway

MicroRNA-3163 targets ADAM-17 and enhances the sensitivity of hepatocellular carcinoma cells to molecular targeted agents

Integrative Bioinformatics Analysis Reveals Potential Target Genes and TNFα Signaling Inhibition by Brazilin in Metastatic Breast Cancer Cells

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