Review of bioanalytical assays for the quantitation of various HDAC inhibitors such as vorinostat, belinostat, panobinostat, romidepsin and chidamine

Suresh, P S; Devaraj, V. C.; Srinivas, Nuggehally R.; Mullangi, Ramesh

doi:10.1002/bmc.3807

Cited by 39 publications

(18 citation statements)

References 31 publications

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“…Histone deacetylases (HDACs) are involved in remodeling nucleosomes and chromatin via removing acetyl group from histone and function as critical transcriptional co-repressors in epigenetic regulation of gene expression [12, 13]. Interestingly, HDAC families are abnormally up-regulated in leukemia [14] and HDAC inhibitors have been used to treat malignant leukemia in clinical studies [15–17]. However, the synergetic regulation of c-Myc and HDAC is not clearly studied in AML.…”

Section: Introductionmentioning

confidence: 99%

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

Gong

Chen

et al. 2016

Oncotarget

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Aberrant activation of c-Myc plays an important oncogenic role via regulating a series of coding and non-coding genes in acute myeloid leukemia (AML). Histone deacetylases (HDACs) can remove acetyl group from histone and regulate gene expression via changing chromatin structure. Here, we found miR-451 is abnormally down-regulated in AML patient samples; c-Myc recruits HDAC3 to form a transcriptional suppressor complex, co-localizes on the miR-451 promoter, epigenetically inhibits its transcription and finally induces its downregulation in AML. Furthermore, our in vitro and in vivo results suggest that miR-451 functions as a tumor suppressor via promoting apoptosis and suppressing malignant cell proliferation. The mechanistic study demonstrated that miR-451 directly targets YWHAZ mRNA and suppresses YWHAZ/AKT signaling in AML. Knockdown of c-Myc results in restoration of miR-451 and inhibition of YWHAZ/AKT signaling. In AML patients, low level of miR-451 is negatively correlated with high levels of c-Myc and YWHAZ, while c-Myc level is positively related to YWHAZ expression. These results suggested that c-Myc⊣miR-451⊣YWHAZ/AKT cascade might play a crucial role during leukemogenesis, and reintroduction of miR-451 could be as a potential strategy for AML therapy.

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Section: Introductionmentioning

confidence: 99%

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

Gong

Chen

et al. 2016

Oncotarget

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“…Dozens of HDAC inhibitors have been developed in recent years [28] . To date, 5 drugs targeting HDAC, including SAHA (Vorinostat), FK228 (Romidepsin), LBH-589 (Panobinostat), PXD101 (Belinostat) and HBI-8000 (Childamide), have been approved worldwide to treat hematological malignancy subtypes [29] . Several clinical trials are ongoing, including but not limited to these five drugs, to expand the application of HDAC inhibitors to solid tumors, especially prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

Marine-derived chromopeptide A, a novel class I HDAC inhibitor, suppresses human prostate cancer cell proliferation and migration

Sun

Wang

et al. 2017

Acta Pharmacol Sin

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Histone deacetylases (HDACs), especially HDAC1, 2, 3 and 4, are abundantly expressed and over-activated in prostate cancer that is correlated with the poor prognosis. Thus, inhibition of HDAC activity has emerged as a potential alternative option for prostate cancer therapy. Chromopeptide A is a depsipeptide isolated from the marine sediment-derived bacterium Chromobacterium sp. HS-13-94; it has a chemical structure highly similar to FK228, a class I HDAC inhibitor that is approved by FDA for treating T-cell lymphoma. In this study, we determined whether chromopeptide A, like FK228, acted as a class I HDAC inhibitor, and whether chromopeptide A could inhibit the growth and migration of human prostate cancer in vitro and in vivo. HDAC enzyme selectivity and kinetic analysis revealed that chromopeptide A selectively inhibited the enzymatic activities of HDAC1, 2, 3 and 8 in a substrate non-competitive manner with comparable IC values for each HDAC member as FK228 in vitro. Importantly, chromopeptide A dose-dependently suppressed the proliferation of human prostate cancer cell lines PC3, DU145 and LNCaP with IC values of 2.43±0.02, 2.08±0.16, and 1.75±0.06 nmol/L, respectively, accompanied by dose-dependent inhibition of HDAC enzymatic activity in PC3 and DU145 cells. Chromopeptide A (0.2-50 nmol/L) caused G/M phase arrest and induced apoptosis in the prostate cancer cell lines. Moreover, chromopeptide A dose-dependently inhibited the migration of PC3 cells. In mice bearing PC3 prostate cancer xenografts, intravenous injection of chromopeptide A (1.6, 3.2 mg/kg, once a week for 18 d) significantly suppressed the tumor growth, which was associated with increased expression levels of Ac-H3 and p21 in tumor tissues. Our results identify chromopeptide A as a novel class I HDAC inhibitor and provide therapeutic strategies that may be implemented in prostate cancer.

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“…Therefore, label‐free analytical approaches are desirable in order to provide a more accurate assessment of tumour drug uptake. LC‐MS/MS is a commonly used label‐free method to measure the amount of a drug in tissues (Sharma et al, ; Suresh et al, ). However, the homogenization of tissues prior to analysis results in the loss of information on drug spatial distribution.…”

Section: Introductionmentioning

confidence: 99%

Heterogeneous distribution of alectinib in neuroblastoma xenografts revealed by matrix‐assisted laser desorption ionization mass spectrometry imaging: a pilot study

Ryu¹,

Hayashi

Aikawa

et al. 2017

British J Pharmacology

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BACKGROUND AND PURPOSEThe penetration of the anaplastic lymphoma kinase (ALK) inhibitor alectinib in neuroblastomas and the relationship between alectinib and ALK expression are unknown. The aim of this study was to perform a quantitative investigation of the inter-and intratumoural distribution of alectinib in different neuroblastoma xenograft models using matrix-assisted laser desorption ionization MS imaging (MALDI-MSI). EXPERIMENTAL APPROACHThe distribution of alectinib in NB1 (ALK amplification) and SK-N-FI (ALK wild-type) xenograft tissues was analysed using MALDI-MSI. The abundance of alectinib in tumours and intra-tumoural areas was quantified using ion signal intensities from MALDI-MSI after normalization by correlation with LC-MS/MS. KEY RESULTSThe distribution of alectinib was heterogeneous in neuroblastomas. The penetration of alectinib was not significantly different between ALK amplification and ALK wide-type tissues using both LC-MS/MS concentrations and MSI intensities. Normalization with an internal standard increased the quantitative property of MSI by adjusting for the ion suppression effect. The distribution of alectinib in different intra-tumoural areas can alternatively be quantified from MS images by correlation with LC-MS/MS. CONCLUSION AND IMPLICATIONSThe penetration of alectinib into tumour tissues may not be homogenous or influenced by ALK expression in the early period after single-dose administration. MALDI-MSI may prove to be a valuable pharmaceutical method for elucidating the mechanism of action of drugs by clarifying their microscopic distribution in heterogeneous tissues. AbbreviationsALK, anaplastic lymphoma kinase; FA, formic acid; ITO, indium titanium oxide; MALDI-MSI, matrix-assisted laser desorption ionization MS imaging; ROIs, regions of interest; RTKIs, RTK inhibitors; RTKs, receptor TKs; α-CHCA, α-cyano-4-hydroxycinnamic acid

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Review of bioanalytical assays for the quantitation of various HDAC inhibitors such as vorinostat, belinostat, panobinostat, romidepsin and chidamine

Cited by 39 publications

References 31 publications

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

c-Myc suppresses miR-451⊣YWTAZ/AKT axis via recruiting HDAC3 in acute myeloid leukemia

Marine-derived chromopeptide A, a novel class I HDAC inhibitor, suppresses human prostate cancer cell proliferation and migration

Heterogeneous distribution of alectinib in neuroblastoma xenografts revealed by matrix‐assisted laser desorption ionization mass spectrometry imaging: a pilot study

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