CALB1 enhances the interaction between p53 and MDM2, and inhibits the senescence of ovarian cancer cells
- Long‑Qiao Cao
- Ya‑Nan Wang
- Ming Liang
- Mei‑Zhou Pan
Affiliations: Reproductive Medical Center, The First People's Hospital of Jining, Jining, Shandong 272100, P.R. China, Reproductive Medical Center, The Second Hospital Affiliated to Shandong University of Traditional Chinese Medicine, Jinan, Shandong 251400, P.R. China, Department of Urology Surgery, The Seventh People's Hospital of Jinan, Jinan, Shandong 251400, P.R. China
- Published online on: April 30, 2019 https://doi.org/10.3892/mmr.2019.10212
Copyright: © Cao
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Numerous studies have demonstrated the association between senescence and cancer. However, the molecular mechanism regulating senescence in ovarian cancer remains unknown. In the present study, the protein expression level of calbindin 1 (CALB1) in ovarian cancer was examined using western blot and immunohistochemistry. The function of CALB1 in ovarian cancer cells was examined using MTT assay, anchorage‑independent growth assay and senescence assay. The molecular mechanisms underlying CALB1 function were investigated using immunoprecipitation and pull‑down assays. In the present study, the expression of CALB1 was found to be increased in ovarian cancer. Overexpression of CALB1 promoted the proliferation and colony formation of ovarian cancer cells and inhibited senescence by modulating the expression levels of p21 and p27. Knockdown of CALB1 inhibited the proliferation and colony formation of ovarian cancer cells. Mechanistically, co‑immunoprecipitation assays revealed that CALB1 interacts with MDM2 proto‑oncogene (MDM2) and promoted the interaction between p53 and MDM2. Collectively, the present study suggested that CALB1 may act as an oncogene in ovarian cancer by inhibiting the p53 pathway.