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Status |
Public on Mar 12, 2015 |
Title |
Gene expression profiling of metastatic lung cancer cell lines |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
During malignant disease progression, the extracellular matrix (ECM) of epithelial tumors accumulates inter-molecular cross-links between collagen strands; these cross-links enhance ECM stiffness and trigger tumor cell invasion and dissemination, but the mechanisms that regulate intra-tumoral collagen maturation have not been fully defined. Using a new mouse model of metastatic lung adenocarcinoma driven by mutant K-ras expression and Cdkn1a inactivation, we showed that tumor cell invasion and metastasis are driven by high expression of lysyl hydroxylase 2 (LH2), an enzyme that hydroxylates telomeric lysine (Lys) residues on collagen.
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Overall design |
We interbred KrasLA1 mice, which develop non-metastatic lung adenocarcinomas at 8-10 months of age because of the expression of a somatically activated K-rasG12D allele, with Cdkn1a-/- mice, which develop sarcomas and B cell lymphomas because of depletion of p21. Cohorts were generated that had neither, either, or both mutant alleles. KrasLA1 mice that were p21-deficient (KC mice) had a shorter mean time to death than did p21-replete ones. We established cell lines from the tumors, and compared cell lines from highly metastatic tumors with those from poorly metastatic tumors.
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Contributor(s) |
Chen Y, Kurie J, Zhang Y, Creighton C |
Citation(s) |
25664850 |
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Submission date |
Jul 29, 2013 |
Last update date |
Feb 11, 2019 |
Contact name |
Chad Creighton |
E-mail(s) |
creighto@bcm.tmc.edu
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Organization name |
Baylor College of Medicine
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Department |
Biostatistics, Ducan Cancer Center
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Street address |
One Baylor Plaza, Mail Stop: BCM305
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City |
Houston |
State/province |
TX |
ZIP/Postal code |
77030 |
Country |
USA |
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Platforms (1) |
GPL1261 |
[Mouse430_2] Affymetrix Mouse Genome 430 2.0 Array |
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Samples (12)
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Relations |
BioProject |
PRJNA213622 |