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

Abstract

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.

Elevated expression of CD93 promotes angiogenesis and tumor growth in nasopharyngeal carcinoma

“…For NPC tissues, the staining intensity was categorized as strong (2), weak (1), or negative (0) semiquantitatively using the following scale: 0, 0% of cells; 1, 1e25% of cells; 2, 26e50% of cells; 3, 51e75% of cells; and 4, 76e100% of cells. The scoring results of intensity and extent were multiplied as described previously [19]. The samples with a final score <4 were regarded as CD93 negative or weak expression and 4e8 were determined as over-expression.…”

ADAM10 and ADAM17 cleave PD-L1 to mediate PD-(L)1 inhibitor resistance

“…High expression of one or both of these closely related metzincin metalloproteinases portends unfavorable outcomes in biliary, breast, cervical, gastric, hepatocellular, lung, nasopharyngeal, ovarian, pancreatic, skin, and urothelial malignancies. [1][2][3][4][5] They also predict treatment resistance in breast, colorectal, hepatocellular, and lung cancers. [6][7][8][9] Long-standing dogma held that metalloproteases contribute to tumor growth and metastasis through enzymatic degradation of the extracellular matrix and tumor cell attachments.…”

ADAM10 promotes cell growth, migration, and invasion in osteosarcoma via regulating E-cadherin/β-catenin signaling pathway and is regulated by miR-122-5p

“…β-catenin could dissociatd from the cytoplasmic tail of E-cadherin and its translocation into the nucleus to regulate the expression of certain genes [31]. In addition, thorsten et al [12] found that ADAM10 mediated E-cadherin shedding and regualted β-catenin translocation. In aother study, ADAM10 decreased E-cadherin protein level and inhibited β-catenin pathway in hepatocellular carcinoma [32].…”

“…The previous studies revealed that the expression of ADAM10 was overexpressed in a variety of tumors including liver cancer [5], melanoma [6], gastric cancer [7], lung cancer [8], pancreatic cancer [9], and bladder cancer [10]. In addition, the silencing of ADAM10 inhibited significantly cell growth and metastasis [11][12][13]. Thorsten Maretzky et al [14] found that the shedding of E-cadherin caused by ADAM10 regulated the β-catenin subcellular localization and its downstream genes.…”