ArticleOncotarget2017
LKB1 loss cooperating with BRAF V600E promotes melanoma cell invasion and migration by up-regulation MMP-2 via PI3K/Akt/mTOR pathway.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Multidrug resistance in the standardized treatment of colon cancer harboring a rare fibrosarcoma B-type (BRAF) p.N581I mutation: a case report.Frontiers in oncology · 2023Article
- Role ofOncology letters · 2022Review
- Review
- Article
- Article
- Loss of Spry1 reduces growth of BRAFCell death & disease · 2020Article
- lncRNA MIAT promotes cell invasion and migration in esophageal cancer.Experimental and therapeutic medicine · 2020Article
- Analysis of candidate genes expected to be essential for melanoma surviving.Cancer cell international · 2020Article
- HPV16 E6/E7 promote the translocation and glucose uptake of GLUT1 by PI3K/AKT pathwayTherapeutic advances in chronic disease · 2020Article
- The Chemosensory Function of Primary Cilia Regulates Cholangiocyte Migration, Invasion, and Tumor Growth.Hepatology (Baltimore, Md.) · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
The serine/threonine kinase LKB1, act as a tumor suppressor, has been reported in several sporadic cancers. However, how the loss of LKB1 promotes melanoma invasion and metastasis remains incompletely understood. In this study, we inactivated LKB1expression by RNA interference in BRAF mutation and wild type melanoma cells respectively. We found LKB1 inactivation cooperate with BRAF V600E lead to melanoma cells more aggressive by a series of experiments including wound scratch test, Transwell assay. While single alteration, either LKB1 loss or BRAF V600E, fails to enhance melanoma cells invasion ability. Mechanistically, LKB1 loss synergism with BRAF V600E resulted in the activation of the PI3K/Akt/mTOR signaling pathway and significant up-regulation expression of MMP-2. In addition, LKB1 expression in human melanoma tissues was negatively associated with MMP-2 expression in the presence of BRAF V600E. Thus, our findings indicate a probable explanation on LKB1 function as a tumor suppressor in melanoma and a new therapeutic strategy for melanoma by targeting on BRAF and LKB1 together.
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