It was shown that HT-29 cells may promote VEGF-C, VEGF-D and VEGFR-3 secreted from tumor and/or stromal cells or indirectly promote VEGF-A and VEGFR-2 secreted from tumor and/or stromal cells, so accelerate the lymphatic tube formation of HDLECs, and the lymphangiogenesis and tumor growth of the in-situ colonic xenografts; NCTD or in combination with mF4-31C1 or Sorafenib markedly downregulated the expression of VEGF-C, VEGF-D and VEGFR-3 other than VEGF-A and VEGFR-2 proteins/mRNAs of the co-culture system in vitro and the in-situ colonic xenografts in vivo. The gene discussed is VEGFC; the disease is neoplasm.