CEMIP was initially identified as an inner-ear specific
protein in which three-point mutations cause folding changes in
protein structure associated with non-syndromic
hearing loss. CEMIP was also involved in other cellular activities, such as
hyaluronan depolymerization independent of CD44 and other hyaluronidases. Growing evidence has demonstrated that CEMIP is involved in the progression of various
tumors. However, whether the oncogenic effects of CEMIP relies on its enzymatic activity remain elusive. CEMIP is significantly related to
metastasis and poor prognosis in patients with various
tumors, suggesting that CEMIP is a potential, highly specific diagnostic
tumor marker. Most preclinical experiments have shown that the overexpression of CEMIP in
tumors mainly affects the adhesion,
metastasis, and invasion of
tumor cells and EMT. Other studies have also demonstrated that CEMIP can promote a variety of
tumor processes by affecting
tumor proliferation, dedifferentiation, and the tumor microenvironment. In terms of molecular mechanisms, existing research has shown that CEMIP mainly affects the WNT and EGFR signaling pathways. In addition, a variety of
miRNAs have been shown to inhibit CEMIP in
tumors. This paper elaborates on the clinical characteristics and regulatory dysfunction of CEMIP in different
cancers. CEMIP provides a new potential target for
therapy of multiple
tumors, which is worthy of further study.