Linifanib (ABT-869), enhances cytotoxicity with poly (ADP-ribose) polymerase inhibitor, veliparib (ABT-888), in head and neck carcinoma cells

Hsu, Heng-Wei; Necochea-Campion, Rosalia de; Williams, Vonetta M.; Duerksen-Hughes, Penelope J.; Simental, Alfred; Ferris, Robert L.; Chen, Chien-Shing; Mirshahidi, Saied

doi:10.1016/j.oraloncology.2014.03.006

Cited by 11 publications

(6 citation statements)

References 36 publications

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“…As such, new PBK inhibitors for cancer treatment are needed. In this study, we screened 31 drugs that potentially target PBK and identified several candidates including linifanib, which is used in the treatment of LIHC, COAD, STAD, NSCLC, and HNSC ( Hsu et al, 2014 ; Chen et al, 2016 ; Horinouchi, 2016 ; Chan et al, 2017 ; Han et al, 2021 ); neratinib, which is used in BRCA ( Saura et al, 2021 ); erlotinib and gefitinib, which are used in NSCLC ( Yang et al, 2017 ); and BMS-536924, which is used in GBM and ESCA ( Adachi et al, 2014 ; Zhou, 2015 ). The anticancer effect of these drugs may be related to PBK inhibition.…”

Section: Discussionmentioning

confidence: 99%

Omics- and Pharmacogenomic Evidence for the Prognostic, Regulatory, and Immune-Related Roles of PBK in a Pan-Cancer Cohort

Liu

Xiang

Peng

et al. 2021

Front. Mol. Biosci.

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PDZ-binding kinase (PBK) is known to regulate tumor progression in some cancer types. However, its relationship to immune cell infiltration and prognosis in different cancers is unclear. This was investigated in the present study by analyzing data from TCGA, GEO, GETx, TIMER, CPTAC, GEPIA2, cBioPortal, GSCALite, PROGNOSCAN, PharmacoDB, STRING, and ENCORI databases. PBK was overexpressed in most tumors including adenocortical carcinoma (hazard ratio [HR] = 2.178, p < 0.001), kidney renal clear cell carcinoma (KIRC; HR = 1.907, p < 0.001), kidney renal papillary cell carcinoma (HR = 3.024, p < 0.001), and lung adenocarcinoma (HR = 1.255, p < 0.001), in which it was associated with poor overall survival and advanced pathologic stage. PBK methylation level was a prognostic marker in thyroid carcinoma (THCA). PBK expression was positively correlated with the levels of BIRC5, CCNB1, CDC20, CDK1, DLGAP5, MAD2L1, MELK, PLK1, TOP2A, and TTK in 32 tumor types; and with the levels of the transcription factors E2F1 and MYC, which regulate apoptosis, the cell cycle, cell proliferation and invasion, tumorigenesis, and metastasis. It was also negatively regulated by the microRNAs hsa-miR-101-5p, hsa-miR-145-5p, and hsa-miR-5694. PBK expression in KIRC, liver hepatocellular carcinoma, THCA, and thymoma was positively correlated with the infiltration of immune cells including B cells, CD4+T cells, CD8+ T cells, macrophages, monocytes, and neutrophils. The results of the functional enrichment analysis suggested that PBK and related genes contribute to tumor development via cell cycle regulation. We also identified 20 drugs that potentially inhibit PBK expression. Thus, PBK is associated with survival outcome in a variety of cancers and may promote tumor development and progression by increasing immune cell infiltration into the tumor microenvironment. These findings indicate that PBK is a potential therapeutic target and has prognostic value in cancer treatment.

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Section: Discussionmentioning

confidence: 99%

Omics- and Pharmacogenomic Evidence for the Prognostic, Regulatory, and Immune-Related Roles of PBK in a Pan-Cancer Cohort

Liu

Xiang

Peng

et al. 2021

Front. Mol. Biosci.

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“…HSC-2, Ca9-22 and CAL27 cells were pre-treated with increasing concentrations of ABT888 (15 µM, 30 µM and 60 µM) or cisplatin (5 µM, 10 µM, 15 µM and 20 µM) in order to assess high concentrations with high toxicity on cell viability. After 24 h, cells were incubated at 37 • C with MTT (0.2 mg/mL) for 1 h. The concentration of Veliparib 60 µM was chosen according to previous studies [28]. The medium was removed by aspiration and the cells lysed with DMSO (100 µL).…”

Section: Mtt Assaymentioning

confidence: 99%

Poly (ADP-Ribose) Polymerase Inhibitor, ABT888, Improved Cisplatin Effect in Human Oral Cell Carcinoma

et al. 2021

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Cisplatin is one of the chemotherapeutic drugs used for the management of oral carcinoma, in which combined therapies are estimated to exert superior therapeutic efficacy compared with monotherapy. It is known that poly(ADP-ribosyl)ation is implicated in a multiplicity of cellular activities, such as DNA repair and cell death. Based on these, PARP inhibitors are used for the treatment of cancers; however, the capacity of PARP inhibitors associated to anti-cancer drugs have not been completely assessed in oral carcinoma. Here, we evaluated the effects of PARPi veliparib (ABT888) in combination with cisplatin on the survival of three human oral cancer cell lines HSC-2, Ca9-22 and CAL27 and we observed the effects of ABT888 alone or in combination with cisplatin on apoptosis and DNA damage repair mechanism. The results obtained showed that ABT888 induces a cytotoxicity effect on cell viability increasing the apoptotic pathway as well as DNA strand break; moreover, our results displayed the effects with cisplatin in a dose-dependent manner. Therefore, our results indicate PARP inhibitors as adjuvants for therapeutic strategy of oral cancer.

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“…Etemadmoghadam and co-workers have attempted to understand the SL interaction between CCNE1 amplification and the impaired BRCA1 function [45]. They have demonstrated the sensitivity of CCNE1-amplified cancer cells on bortezomib (proteasome inhibitor) and hypothesized that CCNE1 amplification and Hsu and co-workers have reported that linifanib (ABT869), a multireceptor tyrosine kinase inhibitor, inhibited radiosensitized head and neck squamous cell carcinoma cells (HNSCC) [47]. They evaluated the PARPi, veliparib (ABT888) in combination with linifanib (ABT869) in HNSCC and showed an increase in inhibition of cell growth and onset of apoptosis.…”

Section: Parp Inhibitors In Dna Damage Responsementioning

confidence: 99%

Embracing synthetic lethality of novel anticancer therapies

Kamal¹,

Shaik

Malik

2015

Expert Opinion on Drug Discovery

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Most of the currently used chemotherapeutic agents will destroy cells irrespective of whether they are cancer cells or fast growing normal cells; but SL is one of the approaches being developed with potential as a selective cancer therapy. PARP inhibitors, such as olaparib, are useful in BRCA mutated cancer cells and are also used in combination with other drug to enhance their efficacy. Research on PARP inhibitors is progressing at a good pace but there are still some significant challenges that must be addressed.

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Linifanib (ABT-869), enhances cytotoxicity with poly (ADP-ribose) polymerase inhibitor, veliparib (ABT-888), in head and neck carcinoma cells

Cited by 11 publications

References 36 publications

Omics- and Pharmacogenomic Evidence for the Prognostic, Regulatory, and Immune-Related Roles of PBK in a Pan-Cancer Cohort

Omics- and Pharmacogenomic Evidence for the Prognostic, Regulatory, and Immune-Related Roles of PBK in a Pan-Cancer Cohort

Poly (ADP-Ribose) Polymerase Inhibitor, ABT888, Improved Cisplatin Effect in Human Oral Cell Carcinoma

Embracing synthetic lethality of novel anticancer therapies

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