Loading patent…
AssigneeIndustry-University Cooperation Foundation Hanyang University Erica Campus
InventorsHyungshin YIM, Jung-Won PARK, Da-Eun KIM
Estimating the term…
The present invention is to confirm that PLK1 induces tumor formation and cancer metastasis through IGFBP5 phosphorylation, and provide an IGFBP5 mutant in which a region phosphorylated by PLK1 is mutated and a vector expressing same. The IGFBP5 mutant of the present invention maintains a binding ability to PLK1, and thus binds to PLK1 overexpressed competitively with wild-type IGFBP5 in cancer cells, thereby making it possible to inhibit tumor formation and cancer metastasis, and the provision of a vector expressing the mutant in cancer cells can inhibit cancer mobility and invasiveness and inhibit tumor formation. The mutant of the present invention is safe because it does not affect the inherent function of IGFBP5 in normal cells, and thus can be useful in the treatment of various diseases caused by abnormal cell growth, especially degenerative diseases such as primary and metastatic solid cancer and leukemia.
An IGFBP5 mutant protein in which an amino acid residue at position 265 and/or 269 of IGFBP5 of SEQ ID NO:
A pharmaceutical composition for cancer prevention or treatment comprising an RNA for inhibiting IGFBP5 expression or a vector expressing the RNA.
Dependencies are inferred from the claim text.