Weiske et al. [52] showed that FHIT interacts with the C-terminus of β-catenin and negatively regulates transcription of target genes such as cyclin D1, MMP-14 and survivin. In addition, ectopic activation of FHIT in FHIT-deficient H1299 cells significantly reduced the invasive potential of tumor cells by down-regulating expression of RhoC, a potential marker of tumor cell invasion and metastases [53]. Here, CCND1 is linked to neoplasm.