Silencing ADAM10 inhibits the in vitro and in vivo growth of hepatocellular carcinoma cancer cells

Liu, Songyang; Zhang, Wei; Li, Kai; Bai, Jing; Wang, Guangyi

doi:10.3892/mmr.2014.2652

Cited by 29 publications

(31 citation statements)

References 28 publications

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“…established that downregulation of ADAM10 in HepG2 cells using RNA silencing significantly suppressed cell proliferation, migration, and invasion in vitro , and tumor growth in vivo . Furthermore, silencing ADAM10 decreased constitutive phosphorylation of phosphoinositide 3‐kinase (PI3K) and Akt, which indicates that ADAM10 is involved in the activation of the PI3K/Akt signaling pathway . In addition, Endres et al .…”

Section: Discussionmentioning

confidence: 98%

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Effects of ADAM10 upregulation on progression, migration, and prognosis of nasopharyngeal carcinoma

et al. 2015

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A disintegrin and metalloprotease 10 (ADAM10) is a typical member of the ADAMs family, which has been reported to be upregulated in various types of cancers and contribute to cancer progression and metastasis. However, little is known about the role of ADAM10 in nasopharyngeal carcinoma (NPC). The purpose of this study is to explore ADAM10 expression status and its biological functions in NPC. We first examined the expression of ADAM10 in NPC tissues and cell lines by immunohistochemistry, Western blotting, PCR, and immunofluorescence analysis. We observed that ADAM10 was significantly elevated in NPC and its expression level was correlated with T classification (P = 0.044), distant metastasis (P = 0.016), TNM clinical stage (P = 0.013), and proliferation marker Ki‐67 expression (P = 0.001). Patients with NPC with high expression of ADAM10 had shorter overall survival rates. In addition, knockdown of ADAM10 by RNAi was found to inhibit the CNE‐2 cell proliferation and migration. Our findings hinted that overexpression of ADAM10 promotes the progression and migration of NPC, which makes it a potential therapeutic target for the treatment of tumor metastases in NPC.

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Section: Discussionmentioning

confidence: 98%

“…ADAM10 has been reported to be overexpressed in various malignancies and to be involved in cancer progression . For example, Liu et al . established that downregulation of ADAM10 in HepG2 cells using RNA silencing significantly suppressed cell proliferation, migration, and invasion in vitro , and tumor growth in vivo .…”

Section: Discussionmentioning

confidence: 99%

Effects of ADAM10 upregulation on progression, migration, and prognosis of nasopharyngeal carcinoma

et al. 2015

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“…Silencing inhibits the in vitro and in vivo growth of hepatocellular carcinoma cells (Liu, Zhang, Liu, Ji, & Wang, ),…”

Section: A Brief History Of Earlier Studies Of Aneuploidy and Admentioning

confidence: 99%

“Amyloid‐beta accumulation cycle” as a prevention and/or therapy target for Alzheimer's disease

et al. 2020

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The cell cycle and its regulators are validated targets for cancer drugs. Reagents that target cells in a specific cell cycle phase (e.g., antimitotics or DNA synthesis inhibitors/replication stress inducers) have demonstrated success as broad‐spectrum anticancer drugs. Cyclin‐dependent kinases (CDKs) are drivers of cell cycle transitions. A CDK inhibitor, flavopiridol/alvocidib, is an FDA‐approved drug for acute myeloid leukemia. Alzheimer's disease (AD) is another serious issue in contemporary medicine. The cause of AD remains elusive, although a critical role of latent amyloid‐beta accumulation has emerged. Existing AD drug research and development targets include amyloid, amyloid metabolism/catabolism, tau, inflammation, cholesterol, the cholinergic system, and other neurotransmitters. However, none have been validated as therapeutically effective targets. Recent reports from AD‐omics and preclinical animal models provided data supporting the long‐standing notion that cell cycle progression and/or mitosis may be a valid target for AD prevention and/or therapy. This review will summarize the recent developments in AD research: (a) Mitotic re‐entry, leading to the “amyloid‐beta accumulation cycle,” may be a prerequisite for amyloid‐beta accumulation and AD pathology development; (b) AD‐associated pathogens can cause cell cycle errors; (c) thirteen among 37 human AD genetic risk genes may be functionally involved in the cell cycle and/or mitosis; and (d) preclinical AD mouse models treated with CDK inhibitor showed improvements in cognitive/behavioral symptoms. If the “amyloid‐beta accumulation cycle is an AD drug target” concept is proven, repurposing of cancer drugs may emerge as a new, fast‐track approach for AD management in the clinic setting.

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“…6 In this study, we first demonstrated that EGCG induced HepG2 and PC12 apoptosis and regulated apoptosis-related proteins Bax and Bcl-2 expression. 12 These data indicated that EGCG induces tumour cells apoptosis via not only reduces APP, but also decreases ADAM10. 6 To our surprise, EGCG also decreased ADAM10 level, a member of the ADAM family involved in multiple cellular processes such as cell proliferation, differentiation, migration and invasion.…”

Section: Discussionmentioning

confidence: 85%

A novel role of HuR in ‐Epigallocatechin‐3‐gallate (EGCG) induces tumour cells apoptosis

Jian

Fang

Chen

et al. 2019

J Cellular Molecular Medi

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Silencing ADAM10 inhibits the in vitro and in vivo growth of hepatocellular carcinoma cancer cells

Cited by 29 publications

References 28 publications

Effects of ADAM10 upregulation on progression, migration, and prognosis of nasopharyngeal carcinoma

Effects of ADAM10 upregulation on progression, migration, and prognosis of nasopharyngeal carcinoma

“Amyloid‐beta accumulation cycle” as a prevention and/or therapy target for Alzheimer's disease

A novel role of HuR in ‐Epigallocatechin‐3‐gallate (EGCG) induces tumour cells apoptosis

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