Because of the importance of the LIS1 gene in regulating cytoplasmic dynein and dynactin functions, it is necessary to analyze the spindle assembly in LIS1-transformed cells; this analysis may provide insight into the mechanism by which LIS1 induces tumorigenesis. We observed a variety of mitotic defects, including impaired or multipolar spindles and chromosome mis-segregations in LIS1-knockdown PD153035 hydrochloride ( Fig. 4). We speculated that cellular transformation caused by impaired LIS1 is directly linked to its role in mitosis. However, whether reduced LIS1 expression can initiate spontaneous liver tumor formation in vivo requires further investigation.
Acknowledgments
This work was supported by Grants from the cephalization National Key S&T Special Project of China (Nos. 2009ZX09103-686, 2008ZX10002-017, and 2008ZX10002-020).
Appendix A. Supplementary data
Supplementary Figure 1.
The LIS1 staining pictures including 90 pairs of tumor cases in the Tissue Microarray. This microarray consists of 88 pairs of HCC, among them 6 cases of HCC accompanied by fatty liver (FL), and 2 pairs of Cholangiocarcinoma (CC). (T) HCC tissues; (N) paired normal liver tissues. The mark in the left corner was the serial number of each case in the slide. Scale bar: 200 μM. The detailed quantitative density was measured and summarized in Table S1.
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Such low level of genetic differentiation
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