These authors contribute equally to this work.
Version of Record online: 4 DEC 2012
Copyright © 2012 American Association for the Study of Liver Diseases
Volume 56, Issue 6, pages 2242–2254, December 2012
How to Cite
Zhou, S.-L., Dai, Z., Zhou, Z.-J., Wang, X.-Y., Yang, G.-H., Wang, Z., Huang, X.-W., Fan, J. and Zhou, J. (2012), Overexpression of CXCL5 mediates neutrophil infiltration and indicates poor prognosis for hepatocellular carcinoma. Hepatology, 56: 2242–2254. doi: 10.1002/hep.25907
Potential conflict of interest: Nothing to report.
Jointly supported by National Natural Science Funds of China (No. 30972949; No. 30972906), the National Basic Research Program of China (973 Program) (2011CB504001), Shanghai Key-Tech Research & Development Program (No. 09411951700), and Program of Shanghai Excellent Subject Leaders (No. 10XD1401200).
- Issue online: 4 DEC 2012
- Version of Record online: 4 DEC 2012
- Accepted manuscript online: 18 JUN 2012 11:58AM EST
- Manuscript Accepted: 3 JUN 2012
- Manuscript Received: 16 JAN 2012
- National Natural Science Funds of China. Grant Numbers: 30972949, 30972906
- National Basic Research Program of China. Grant Numbers: 973 Program, 2011CB504001
- Shanghai Key-Tech Research & Development Program. Grant Number: 09411951700
- Program of Shanghai Excellent Subject Leaders. Grant Number: 10XD1401200
Additional Supporting Information may be found in the online version of this article.
|HEP_25907_sm_SuppFig1.tif||1735K||Supporting Information Figure 1. CXCL5 promotes migration and invasion of HCC cells in vitro. (A) In wound-healing migration assays, microscopic examination at 24 hours post-wounding revealed a significant delay in the wound closure rate of HCCLM3-shRNA-CXCL5 and MHCC97H-shRNA-CXCL5 cells compared with the control cell lines, whereas, HepG2-CXCL5 and PLC/PRF/5-CXCL5 cells had a significant increase in the wound closure rate compared with control cell lines (B). (C) In vitro invasive assays showed that the numbers of invasive HCCLM3-Mock and MHCC97H-Mock cells were significantly higher than those of HCCLM3-shRNA-CXCL5 and MHCC97H-shRNA-CXCL5 cells. (D) The numbers of invasive HepG2-CXCL5 and PLC/PRF/5-CXCL5 cells were significantly higher than those of HepG2-Mock and PLC/PRF/5-Mock cells. Magnification, 100× (A-B) and 200× (C-D).|
|HEP_25907_sm_SuppFig2.tif||197K||Supporting Information Figure 2. CXCL5 attracts neutrophils in vitro. (A) In vitro transwell assays show that CXCL5 induces concentration-dependent migration of neutrophils. (B) Western blot analysis of p-Akt and p-p65 in response to CXCL5.|
|HEP_25907_sm_SuppFig3.tif||378K||Supporting Information Figure 3. Statistical analysis of tumor volume, intratumoral neutrophil number, and pulmonary metastases in xenografts from nude mice. (A) The tumor volume of the xenograft in each nude mouse group. (B) The number of intratumoral neutrophils in each group of xenograft nude mice. (C-F) All grades of metastatic nodules in lungs of all xenograft nude mice groups.|
|HEP_25907_sm_SuppFig4.tif||9004K||Supporting Information Figure 4. Representative images of Gr1+ intratumoral neutrophils with magnification of the selected areas in Fig. 4. Magnification, 200×.|
|HEP_25907_sm_SuppFig5.tif||271K||Supporting Information Figure 5. Kaplan-Meier analysis of OS rates (A-B) and cumulative recurrence rates (C-D) in 94 HCCs (cohort 1) with different CXCL5 expression levels.|
|HEP_25907_sm_SuppFig6.tif||315K||Supporting Information Figure 6. The correlation and prognostic value of CXCL5 and intratumoral CD66b+ neutrophils in HCC samples (cohort 3, n=502). (A-C) Prognostic value of CXCL5 expression and intratumoral CD66b by Kaplan-Meier analysis. I, CXCL5Low/intratumoral CD66bLow; II, CXCL5Low/intratumoral CD66bHigh and CXCL5High/intratumoral CD66bLow; III, CXCL5High/intratumoral CD66bHigh. (D) Significant positive correlation between CXCL5 expression and intratumoral CD66b in cancerous tissues, shown with a scatter plot.|
|HEP_25907_sm_SuppFig7.tif||1900K||Supporting Information Figure 7. Representative images of intratumoral lymphocytes. (A) CD3+, (B) CD4+, (C) CD8+, (D) CD45RO+, (E) Foxp3+, and (F) granzyme B+. Magnification, 200×.|
|HEP_25907_sm_SuppTab1.doc||41K||Supporting Information Table 1. Up-regulated at least one-fold of protein phosphorylation after CXCL5 treatment in human neutrophils.|
|HEP_25907_sm_SuppTab2.doc||43K||Supporting Information Table 2. Clinicopathologic characteristics of three cohorts of patients with hepatocellular carcinoma.|
|HEP_25907_sm_SuppTab3.doc||51K||Supporting Information Table 3. Correlation between the factors and clinicopathologic characteristics in HCC (cohort 1, n=94).|
|HEP_25907_sm_SuppTab4.doc||50K||Supporting Information Table 4. Univariate and multivariate analyses of prognostic factors in HCC (cohort 1, n=94).|
|HEP_25907_sm_SuppTab5.doc||48K||Supporting Information Table 5. Correlation between the factors and clinicopathologic characteristics in HCC (cohort 3, n=502).|
|HEP_25907_sm_SuppTab6.doc||60K||Supporting Information Table 6. Univariate and multivariate analyses of prognostic factors in HCC (cohort 3, n=502).|
|HEP_25907_sm_SuppTab7.doc||42K||Supporting Information Table 7. Univariate analyses of intratumoral lymphocytes in HCC (cohort 2, n=323 and cohort 3, n=502).|
|HEP_25907_sm_SuppTab8.doc||40K||Supporting Information Table 8. Descriptive statistics of immunohistochemical variables of intratumoral lymphocytes in HCC and correlations with CD66b/CXCL5 (cohort 2, n=323 and cohort 3, n=502).|
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