Tags

Type your tag names separated by a space and hit enter

RETRACTED ARTICLE

Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway.
J Cell Biochem. 2018 12; 119(12):9899-9909.JC

Abstract

Osteosarcoma (OS) is an aggressive malignant tumor of bone, which often occurs in children and adolescents. Currently, the effective method for the treatment of OS is still limited. The study aimed to investigate the synergistic antitumor effect of inositol polyphosphate-4-phosphatase, type-II (INPP4B) and rucaparib on OS cells. The expression levels of INPP4B in OS tissues and OS cell lines were examined by quantitative real-time polymerase chain reaction and Western blot analysis. SaOS2 and U2OS cells were then transfected with overexpression vector of INPP4B or were treated with different concentrations of rucaparib, and cell viability, cell cycle, and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry. Western blot assay uncovered the combined effects of INPP4B and rucaparib on cell cycle, apoptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signal pathway. Further, the tumor formation was examined in vivo. Results showed that INPP4B was low expressed in OS tissues and in OS cell lines. INPP4B overexpression significantly decreased cell viability and induced apoptosis in SaOS2 and U2OS cells. Additionally, rucaparib remarkably reduced cell viability in a dose-dependent and time-dependent manner. Meanwhile, rucaparib suppressed cell cycle progression in the S phase and promoted apoptosis in a dose-dependent manner. Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells. Finally, combination of INPP4B overexpression and rucaparib inhibited tumor formation in vivo. The study demonstrated that INPP4B and rucaparib exhibited synergistic antitumor effect by regulating PI3K/AKT pathway in OS cells.

Authors+Show Affiliations

Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.Department of Pathology, The Second Hospital of Shandong University, Jinan, China.Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.Department of Spinal Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, China.

Pub Type(s)

Journal Article
Retracted Publication

Language

eng

PubMed ID

30132953

Citation

Li, Dong, et al. "Inositol Polyphosphate-4-phosphatase Type II and Rucaparib Treatment Inhibit the Growth of Osteosarcoma Cells Dependent On Phosphoinositide 3-kinase/protein Kinase B Pathway." Journal of Cellular Biochemistry, vol. 119, no. 12, 2018, pp. 9899-9909.
Li D, Yang J, Ma H, et al. Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway. J Cell Biochem. 2018;119(12):9899-9909.
Li, D., Yang, J., Ma, H., Sun, C., & Feng, R. (2018). Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway. Journal of Cellular Biochemistry, 119(12), 9899-9909. https://doi.org/10.1002/jcb.27311
Li D, et al. Inositol Polyphosphate-4-phosphatase Type II and Rucaparib Treatment Inhibit the Growth of Osteosarcoma Cells Dependent On Phosphoinositide 3-kinase/protein Kinase B Pathway. J Cell Biochem. 2018;119(12):9899-9909. PubMed PMID: 30132953.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inositol polyphosphate-4-phosphatase type II and rucaparib treatment inhibit the growth of osteosarcoma cells dependent on phosphoinositide 3-kinase/protein kinase B pathway. AU - Li,Dong, AU - Yang,Jingyan, AU - Ma,Huanzhi, AU - Sun,Chengliang, AU - Feng,Rongjie, Y1 - 2018/08/21/ PY - 2017/12/29/received PY - 2018/06/25/accepted PY - 2018/8/23/pubmed PY - 2019/12/18/medline PY - 2018/8/23/entrez KW - apoptosis KW - cell viability KW - inositol polyphosphate-4-phosphatase KW - osteosarcoma KW - phosphoinositide 3-kinase/protein kinase B KW - rucaparib KW - type-II (inositol polyphosphate-4-phosphatase) SP - 9899 EP - 9909 JF - Journal of cellular biochemistry JO - J Cell Biochem VL - 119 IS - 12 N2 - Osteosarcoma (OS) is an aggressive malignant tumor of bone, which often occurs in children and adolescents. Currently, the effective method for the treatment of OS is still limited. The study aimed to investigate the synergistic antitumor effect of inositol polyphosphate-4-phosphatase, type-II (INPP4B) and rucaparib on OS cells. The expression levels of INPP4B in OS tissues and OS cell lines were examined by quantitative real-time polymerase chain reaction and Western blot analysis. SaOS2 and U2OS cells were then transfected with overexpression vector of INPP4B or were treated with different concentrations of rucaparib, and cell viability, cell cycle, and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry. Western blot assay uncovered the combined effects of INPP4B and rucaparib on cell cycle, apoptosis and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signal pathway. Further, the tumor formation was examined in vivo. Results showed that INPP4B was low expressed in OS tissues and in OS cell lines. INPP4B overexpression significantly decreased cell viability and induced apoptosis in SaOS2 and U2OS cells. Additionally, rucaparib remarkably reduced cell viability in a dose-dependent and time-dependent manner. Meanwhile, rucaparib suppressed cell cycle progression in the S phase and promoted apoptosis in a dose-dependent manner. Further, combination of INPP4B overexpression and rucaparib declined Myc, cyclin E1 and cyclin D1 expressions, enhanced Bad, Bax, and cleaved-caspase-3 expressions, and blocked PI3K/AKT signal pathway in SaOS2 and U2OS cells. Finally, combination of INPP4B overexpression and rucaparib inhibited tumor formation in vivo. The study demonstrated that INPP4B and rucaparib exhibited synergistic antitumor effect by regulating PI3K/AKT pathway in OS cells. SN - 1097-4644 UR - https://www.unboundmedicine.com/medline/citation/30132953/Inositol_polyphosphate_4_phosphatase_type_II_and_rucaparib_treatment_inhibit_the_growth_of_osteosarcoma_cells_dependent_on_phosphoinositide_3_kinase/protein_kinase_B_pathway_ L2 - https://doi.org/10.1002/jcb.27311 DB - PRIME DP - Unbound Medicine ER -