Lysyl oxidase-like 2 (LOXL2) controls tumor-associated cell proliferation through the interaction with MARCKSL1

Kim, Boh-Ram; Dong, Seung Myung; Seo, Seung Hee; Lee, Ji-Hae; Lee, Jae Myun; Lee, Seung‐Hoon; Rho, Seung Bae

doi:10.1016/j.cellsig.2014.05.010

Cited by 30 publications

(29 citation statements)

References 48 publications

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“…The mechanisms of LOXL2 in cancer have been reported previously as being related to the activation of an epithelial-mesenchymal transition 43 as well as VEGF, 44 HIF-1-α, 45 and the FAK and AKT pathway 26 in different types of cancers. The results of the current study demonstrated that the LOXL2 variant activated the FAK and AKT pathway in HPV-negative HNSCC, with increases in p-FAK, p-AKT T308 , p-AKT S473 , and p-S6.…”

Section: Discussionmentioning

confidence: 91%

A novel splice variant of LOXL2 promotes progression of human papillomavirus–negative head and neck squamous cell carcinoma

Liu

Guo

Sakai

et al. 2019

Cancer

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BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) is one of the most frequently diagnosed cancers worldwide. LOXlike (LOXL) 2 (LOXL2) demonstrates alternative splicing events in patients with human papillomavirus (HPV)-negative HNSCC. The current study explored the role of a dominant LOXL2 variant in HPV-negative HNSCC. METHODS: Expression of the LOXL2 variant was analyzed using The Cancer Genome Atlas cohorts and validated using quantitative reverse transcriptase-polymerase chain reaction in a separate primary tumor set. The authors defined the effect of LOXL2 splice variants in assays for cell proliferation using a cell viability assay and colony formation assay. Cell migration and invasion were examined using a cell scratch assay and transwell cell migration and invasion assay in LOXL2 splice variant gain and loss of expression cells. Western blot analysis and gene set enrichment analysis were used to explore the potential mechanism of the LOXL2 splice variant in HPV-negative HNSCC. RESULTS: Expression of a novel LOXL2 variant was found to be upregulated in The Cancer Genome Atlas HPV-negative HNSCC, and confirmed in the separate primary tumor validation set. Analyses of loss and gain of function demonstrated that this LOXL2 variant enhanced proliferation, migration, and invasion in HPV-negative HNSCC cells and activated the FAK/AKT pathway. A total of 837 upregulated and 820 downregulated genes and 526 upregulated and 124 downregulated pathways associated with LOXL2 variant expression were identified using gene set enrichment analysis, which helped in developing a better understanding of the networks activated by this LOXL2 variant in patients with HPV-negative HNSCC. CONCLUSIONS: The novel LOXL2 variant can promote the progression of HPV-negative HNSCC, in part through FAK/AKT pathway activation, which may provide a new potential therapeutic target among patients with HPV-negative HNSCC. Cancer 2020;126:737-748.

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Section: Discussionmentioning

confidence: 91%

A novel splice variant of LOXL2 promotes progression of human papillomavirus–negative head and neck squamous cell carcinoma

Liu

Guo

Sakai

et al. 2019

Cancer

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“…These data render this approach important for the clinical setting. Although the authors attribute these effects to the extracellular LOXL, previous data on its involvement in cell proliferation and inhibition of apoptotic cell death via focal adhesion kinase/protein kinase B/mechanistic target of rapamycin4 suggest that LOXL2 blockage might have direct effects on hepatic stellate cells (HSC), the main source of collagen 5. However, in the present study, the authors focus only on the contraction of these cells, which is possibly due to either the disintegration of their surrounding ECM or direct effect of LOXL2 inhibition on HSC, or both.…”

mentioning

confidence: 95%

Selective LOXL2 inhibition: potent antifibrotic effects in ongoing fibrosis and fibrosis regression

Magdaleno

Trebicka

2017

Gut

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“…Semelhante a LOX, o aumento da expressão dos demais membros da família das lisil oxidases já foi descrito em diversos tumores (Tabela 1), inclusive correlacionando com prognóstico de pacientes com tumor de ovário, mama, laringe, cabeça e pescoço, pulmão, pâncreas, cólon, reto e melanoma (Xiao & Ge, 2012;, Barker 2012, Kim et al, 2014. Apesar desta grande variedade de tumores nos quais os membros da família das lisil oxidases estão envolvidos, os trabalhos em tumores do sistema nervoso central são ainda escassos.…”

Section: Família Das Lisil Oxidases Como Promotora De Progressão Tumoralunclassified

“…Em câncer de mama, a alta expressão de LOXL2 está associada com um tumor maior agressivo (Peinado et al, 2008, Barry-Hamilton et al, 2010Barker et al, 2011;Moreno-Bueno et al, 2011;Akiri et al, 2003) e também com metástase e menor sobrevida de pacientes com tumor negativo para o receptor de estrógeno (Barker et al, 2011;Ahn et al, 2013;Kim et al, 2014).…”

Section: Família Das Lisil Oxidases Como Promotora De Progressão Tumoralunclassified

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Expressão gênica da família das lisil oxidases e papel funcional de LOX em astrocitomas

Silva¹

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Lysyl oxidase-like 2 (LOXL2) controls tumor-associated cell proliferation through the interaction with MARCKSL1

Cited by 30 publications

References 48 publications

A novel splice variant of LOXL2 promotes progression of human papillomavirus–negative head and neck squamous cell carcinoma

A novel splice variant of LOXL2 promotes progression of human papillomavirus–negative head and neck squamous cell carcinoma

Selective LOXL2 inhibition: potent antifibrotic effects in ongoing fibrosis and fibrosis regression

Expressão gênica da família das lisil oxidases e papel funcional de LOX em astrocitomas

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