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. 2020 Jan;10(1):294-296.
doi: 10.1002/ctm2.36.

Comprehensive genomic profiling of urothelial carcinoma cell lines reveals hidden research bias and caveats

Yongwen Luo  1 , Lingao Ju  2 , Gang Wang  2 , Chen Chen  2 , Yejinpeng Wang  1 , Liang Chen  1 , Yi Zhang  3 , Yu Xiao  1   2 , Xinghuan Wang  1   2   4
Affiliations

Comprehensive genomic profiling of urothelial carcinoma cell lines reveals hidden research bias and caveats

Yongwen Luo et al. Clin Transl Med. 2020 Jan.
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Comprehensive genomic profiling of urothelial carcinoma cell lines reveals hidden research bias and caveats. A, Distance from given target gene to TP53 on KEGG pathway is negatively correlated with RT4 usage. X‐axis: distance to TP53 and FGFR3 (1, 2, and 3 denote direct interacting with TP53, one‐step away from TP53, and two‐step away from TP53, etc.). Y‐axis: PubMed search result number of target gene name with RT4. B, The relative distance from given target gene to TP53 and FGFR3 based on protein‐protein interaction network is correlated with RT4 usage. X‐axis: The difference between target‐gene‐to‐TP53 distance and target‐gene‐to‐FGFR3 distance. A minus number denotes the gene is closer to FGFR3 compared to TP53, and a positive number denotes the gene is closer to TP53 compared to FGFR3. Y‐axis: Frequency of RT4‐containing search result in all PubMed search results with target gene and “bladder cancer cell line.” C, Papers studying FGFR3 pathway are more likely to use RT4 density distribution of the RT4‐containing search result frequency on PubMed for target genes in the KEGG FGFR3‐related signaling pathway or TP53‐related signaling pathway. D, Morphology of 2 BCa patient‐derived CRCs (a‐b). Scale bar is 50 μm. Visually pan‐genome copy number profile (yellow) with sequencing depth of probe region (gray) generated by CNVkit from 2 CRCs (c‐d) and 2 BCa tissue (e‐f) together with BCa cell lines T24 and RT4 (g‐h) showing the significant deviation from genuine BCa cell lines. E, Sequencing evidence for heterogeneity of driver oncogene fusion in SW780 cell line. Top panel showing the raw sequencing reads (yellow, cross‐chromosomal DNA fragments; gray, normal DNA fragments; green, fragments in inverted direction) of FGFR3 (top‐left) and BAIAP2L1 (top‐right) loci. Middle panel showing the chromosomal bands and gene structure, denoting the breakpoint locus. Bottom panel showing the original transcript (Tx) and respective functional domains of each fusion partner gene, and the predicted fusion product transcript with a functional FGFR3 kinase domain and longer C‐termini from BAIAP2L1. DNA fragments in support of fusion consist 7.3% (five in 81) of all sequenced fragments, suggesting that the fusion driver oncogene is lost in a part of cells. F, Sequencing evidence for TACC3‐FGFR3 driver oncogene fusion in RT4 cell line. Panel layout is similar to (E). DNA fragments in support of fusion consist 26.6% (53 in 268) of all sequenced fragments, suggesting that the fusion driver oncogene likely to exist in homogeneous one‐in‐a‐tetraploid cell state or in a heterogeneous manner. Copy number profile (a in panel D), however, did suggest that significant level of mosaicism exists in the RT4 population.
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References

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