AI Article Synopsis
- The study systematically characterized B16-F10 melanoma, a metastatic sub-line from B16-F1 cells, to uncover mechanisms driving metastasis.
- RNA-sequencing and network analyses revealed several overexpressed genes linked to metastasis, including Nr5a1/sf1, Hoxb8, and Ptk7, which showed significantly higher expression in B16-F10 compared to B16-F1.
- Additionally, B16-F10 cells exhibited unique chromosomal aberrations that may contribute to their metastatic behavior, highlighting potential targets for future cancer treatment strategies.
Article Abstract
Aims: We systematically characterized metastatic murine B16-F10 melanoma, a sub-line derived from murine melanoma B16-F1 cells.
Materials And Methods: RNA-sequencing and network analyses (Ingenuity Pathway Analysis) were performed to identify novel potential metastasis mechanisms. Chromosomal aberrations were identified by multicolor fluorescence in situ hybridization (mFISH) using all 21 murine whole chromosome painting probes.
Key Findings: Numerous genes were overexpressed in B16-F10 cells, some of which have been already described as being metastasis-linked. Nr5a1/sf1, a known prognostic marker for adrenal tumors, was 177-fold upregulated in B16-F10 cells compared to B16-F1 cells. Hoxb8 was 75-fold upregulated, which was previously associated with gastric cancer progression and metastasis. Ptk7, which is linked with tumorigenesis and metastasis of esophageal squamous carcinoma, was 67-fold upregulated. B16-F10 cells acquired additional chromosomal aberrations compared to B16-F1 cells, including dic(4)(pter->qter:qter->pter), +dic(6;15), +der(10)t(10;?1;16).
Significance: In addition to well-known metastatic genes, numerous novel genes and genomic aberrations were identified, which may serve as targets for treatment in the future. Transcriptomic and genetic analyses in B16-F10 cells unraveled a range of novel metastasis mechanisms, which may also have important implications for future treatment strategies.
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| http://dx.doi.org/10.1016/j.lfs.2020.118922 | DOI Listing |
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