RNAi-mediated human Nestin silence inhibits proliferation and migration of malignant melanoma cells by G1/S arrest via Akt-GSK3β-Rb pathway

2017 ◽  
Vol 37 (6) ◽  
pp. 895-903
Author(s):  
Xu-hui Yang ◽  
Tian Xia ◽  
Jie Zhang ◽  
Shao-fen Yang ◽  
Hui-xia Tang ◽  
...  
2017 ◽  
Vol 14 (2) ◽  
pp. 931-938 ◽  
Author(s):  
Pingyuan Bu ◽  
Chengqun Luo ◽  
Quanyong He ◽  
Ping Yang ◽  
Xi Li ◽  
...  

2021 ◽  
Author(s):  
Jessica Ceramella ◽  
Chiara La Torre ◽  
Domenico Iacopetta ◽  
Alexia Barbarossa ◽  
Fabrizio Francomano ◽  
...  

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2328 ◽  
Author(s):  
Corinna Kosnopfel ◽  
Tobias Sinnberg ◽  
Birgit Sauer ◽  
Heike Niessner ◽  
Alina Muenchow ◽  
...  

Secreted factors play an important role in intercellular communication. Therefore, they are not only indispensable for the regulation of various physiological processes but can also decisively advance the development and progression of tumours. In the context of inflammatory disease, Y-box binding protein 1 (YB-1) is actively secreted and the extracellular protein promotes cell proliferation and migration. In malignant melanoma, intracellular YB-1 expression increases during melanoma progression and represents an unfavourable prognostic marker. Here, we show active secretion of YB-1 from melanoma cells as opposed to benign cells of the skin. Intriguingly, YB-1 secretion correlates with the stage of melanoma progression and depends on a calcium- and ATP-dependent non-classical secretory pathway leading to the occurrence of YB-1 in the extracellular space as a free protein. Along with an elevated YB-1 secretion of melanoma cells in the metastatic growth phase, extracellular YB-1 exerts a stimulating effect on melanoma cell migration, invasion, and tumourigenicity. Collectively, these data suggest that secreted YB-1 plays a functional role in melanoma cell biology, stimulating metastasis, and may serve as a novel biomarker in malignant melanoma that reflects tumour aggressiveness.


2019 ◽  
Vol 25 ◽  
pp. 8722-8732 ◽  
Author(s):  
Zhaoxia Xia ◽  
Chaoying Yang ◽  
Xiaoxi Yang ◽  
Shuduan Wu ◽  
Zhizhen Feng ◽  
...  

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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