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The role of LOXL2 in tumor progression, immune response and cellular senescence: a comprehensive analysis
LOXL2 , an enzyme belonging to the LOX family, facilitates the cross-linking of extracellular matrix (ECM) elements. However, the roles of the LOXL2 gene in mechanisms of oncogenesis and tumor development have not been clearly defined. In this pan-cancer study, we examined the notable disparity in L...
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Published in: | Discover. Oncology 2024-06, Vol.15 (1), p.245-18, Article 245 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | LOXL2
, an enzyme belonging to the
LOX
family, facilitates the cross-linking of extracellular matrix (ECM) elements. However, the roles of the
LOXL2
gene in mechanisms of oncogenesis and tumor development have not been clearly defined. In this pan-cancer study, we examined the notable disparity in
LOXL2
expression at the mRNA and protein levels among various cancer types and elucidated its interconnected roles in tumor progression, mutational profile, immune response, and cellular senescence. Apart from investigating the hyperexpression of
LOXL2
being related to poorer prognosis in different types of tumors, this study also unveiled noteworthy connections between
LOXL2
and genetic mutations, infiltration of tumor immune cells, and genes in immune checkpoint pathways. Further analysis revealed the participation of
LOXL2
in multiple pathways related to cancer extracellular matrix remodeling and cellular senescence. Moreover, our investigation uncovered that the knockdown and inhibition of
LOXL2
significantly attenuated the proliferation and migration of PC-9 and HCC-LM3 cells. The knock-down and inhibition of
LOXL2
enhanced cellular senescence in lung and liver cancer cells, as confirmed by SA-β-Gal staining and quantitative RT-PCR analyses. This comprehensive analysis offers valuable insights on the functions of
LOXL2
in different types of cancer and its role in regulating the senescence of cancer cells. |
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ISSN: | 2730-6011 2730-6011 |
DOI: | 10.1007/s12672-024-01107-9 |