AHNAK Nucleoprotein 2 Performs a Promoting Role in the Proliferation and Migration of Uveal Melanoma Cells

2019 ◽  
Vol 34 (10) ◽  
pp. 626-633 ◽  
Author(s):  
Mengyun Li ◽  
Yanchen Liu ◽  
Yanling Meng ◽  
Yan Zhu
2019 ◽  
Vol 25 ◽  
pp. 8722-8732 ◽  
Author(s):  
Zhaoxia Xia ◽  
Chaoying Yang ◽  
Xiaoxi Yang ◽  
Shuduan Wu ◽  
Zhizhen Feng ◽  
...  

2020 ◽  
Vol 318 (5) ◽  
pp. C903-C912 ◽  
Author(s):  
Shuai Wu ◽  
Han Chen ◽  
Ling Zuo ◽  
Hai Jiang ◽  
Hongtao Yan

This study explored the effects of the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on the development of uveal melanoma. Moreover, the role of the MALAT1/microRNA-608 (miR-608)/homeobox C4 (HOXC4) axis was assessed by evaluating the proliferation, invasion, and migration, as well as the cell cycle distribution of uveal melanoma in vitro after knocking down MALAT1 or HOXC4 and/or overexpression of miR-608 in uveal melanoma cells (MUM-2B and C918). Moreover, the effects of the MALAT1/miR-608/HOXC4 axis in uveal melanoma in vivo were further evaluated by injecting the C918 cells into the NOD/SCID mice. HOXC4 was found to be a gene upregulated in uveal melanoma, while knockdown of its expression resulted in suppression of uveal melanoma cell migration, proliferation, and invasion, as well as cell cycle progression. In addition, the upregulation of miR-608 reduced the expression of HOXC4 in the uveal melanoma cells, which was rescued by overexpression of MALAT1. Hence, MALAT1 could upregulate the HOXC4 by binding to miR-608. The suppressed progression of uveal melanoma in vitro by miR-608 was rescued by overexpression of MALAT1. Additionally, in vivo assays demonstrated that downregulation of MALAT1 could suppress tumor growth through downregulation of HOXC4 expression via increasing miR-608 in uveal melanoma. In summary, MALAT1 downregulation functions to restrain the development of uveal melanoma via miR-608-mediated inhibition of HOXC4.


2020 ◽  
Vol 16 (8) ◽  
pp. 1205-1218
Author(s):  
Wei Li ◽  
Aiqin Nie ◽  
Qiang Li ◽  
He Cao ◽  
Yinwei Song ◽  
...  

Recent studies have found that chromosome 3 is frequently mutated in metastatic uveal melanoma (UVM), which leads to the loss of BAP1 expression or the weakening of BRCA1-associated protein 1 (BAP1) function and promotes metastasis of uveal melanoma cells. However, the specific signaling pathways that are affected by BAP1 depletion in uveal melanoma remain unclear. Our aim in this study was to verify the effect and regulatory mechanism of BAP1 on uveal melanoma. RT-qPCR and western blotting results showed that BAP1 was significantly down-regulated in OCM-1A cells treated with a BAP1 shRNA vector. MTT, cell scratch and transwell migration assays showed that low expression of BAP1 significantly promoted the proliferation and migration of UVM cells. A total of 269 up-regulated and 807 down-regulated genes were identified from the combined GSE110193 and GSE48863 data sets. These differentially expressed genes are mainly involved in the composition of extracellular matrix and the regulation of the Wnt signaling pathway and are closely related to the cell adhesion pathway. CXCL8, COL5A3, COL11A1, and COL12A1 were among the differentially expressed genes and are closely related to the prognosis of UVM. Therefore, the deletion of BAP1 is closely related to poor prognosis of UVM and is a risk factor for UVM metastasis. The potential targets of BAP1 include CXCL8, COL5A3, COL11A1, and COL12A1. It is believed that BAP1 regulates UVM cell adhesion through these four genes and ultimately regulates tumor development and migration.


2017 ◽  
Vol 37 (6) ◽  
pp. 895-903
Author(s):  
Xu-hui Yang ◽  
Tian Xia ◽  
Jie Zhang ◽  
Shao-fen Yang ◽  
Hui-xia Tang ◽  
...  

Author(s):  
Chun‑Te Lu ◽  
Pui‑Ying Leong ◽  
Ting‑Yi Hou ◽  
Yu‑Ting Kang ◽  
Yan‑Cheng Chiang ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 5301-5320 ◽  
Author(s):  
Eleonora Vighi ◽  
Andreas Rentsch ◽  
Philipp Henning ◽  
Antonella Comitato ◽  
Dorit Hoffmann ◽  
...  

2017 ◽  
Vol 213 (4) ◽  
pp. 400-404 ◽  
Author(s):  
Theresa Meyer ◽  
Andreas Koch ◽  
Eva-Vanessa Ebert ◽  
Barbara Czech ◽  
Martina Mueller ◽  
...  

2021 ◽  
Vol 12 (5) ◽  
Author(s):  
Ting Huang ◽  
Yong-Jie Wang ◽  
Mi-Tao Huang ◽  
Yu Guo ◽  
Li-Chang Yang ◽  
...  

AbstractRecently studies found that APEX1 was abnormally expressed in melanoma, indicating that it might be involved in the development of melanoma. However, the underlying mechanism and the interaction between APEX1 and LINC00470 in melanoma are not clear. Therefore, we aimed to investigate the role of LINC00470 in the development of melanoma in this work. We discovered that LINC00470 was overexpressed in melanoma tissues and cells compared with the adjacent normal tissues and cells by qPCR. The overexpression of LINC00470 promoted the proliferation and migration of melanoma cells. The functional investigation demonstrated that LINC00470 activated the transcription factor, ZNF131, to regulate the APEX1 expression, which finally promoted cell proliferation and migration. In contrast, knockdown of LINC00470 could significantly inhibit the melanoma cell proliferation and migration, and suppress the growth of tumor in vivo. Overexpression of APEX1 could reverse the impact of the silence of LINC00470 in melanoma cells. In summary, our studies revealed that LINC00470 promoted melanoma proliferation and migration by enhancing the expression of APEX1, which indicated that LINC00470 might be a therapeutic target for the treatment of melanoma.


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