Anticancer efficacy of cisplatin and trichostatin A or 5-aza-2′-deoxycytidine on ovarian cancer

Meng, Fanliang; Sun, Guizhi; Zhong, Meifeng; Yu, Yang; Brewer, Molly

doi:10.1038/bjc.2013.10

Cited by 60 publications

(39 citation statements)

References 37 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The demethylation agent 5-AZA is an effective anticancer therapy (24,25). In the current study, 5-AZA treatment rescued the expression of GATA5 mRNA by reversing GATA5 hypermethylation in HCC cell lines.…”

Section: A B C D Ementioning

confidence: 72%

Loss of GATA5 expression due to gene promoter methylation induces growth and colony formation of hepatocellular carcinoma cells

et al. 2015

View full text Add to dashboard Cite

Abstract. GATA5 is a transcription factor that is capable of suppressing the development of various types of human cancer. The present study investigated the expression of GATA5 and GATA4, and examined their roles in the proliferation and colony formation ability of hepatocellular carcinoma (HCC) tissues and cells. The GATA4 and GATA5 expression levels and gene promoter methylation of HCC tissue samples from 38 patients and HCC cell lines were analyzed using reverse transcription-polymerase chain reaction (RT-PCR) and methylation-specific PCR (MSP), respectively. The effects of GATA4 and GATA5 overexpression on the proliferation and colony forming ability of HCC cells were also assessed using cell viability and colony formation assays. A luciferase reporter assay was utilized to investigate the transcriptional interaction of GATA4 and GATA5 with canonical Wnt signaling. The results indicated that the expression levels of GATA4 and GATA5 were lost or reduced following methylation of gene promoters in HCC tissues and cell lines. Treatment with a demethylating agent, 5-aza-2'-deoxycytidine (5-AZA), restored GATA4 and GATA5 expression in HCC cell lines. Furthermore, methylation of the GATA5 promoter was observed to be associated with the age of patients exhibiting HCC. Restoration of GATA4 and GATA5 expression inhibited colony formation and induced apoptosis of HCC cells in vitro. The present study concluded that the expression levels of GATA4 and GATA5 were reduced in HCC tissues and cell lines. Treatment with 5-AZA restored GATA4 and GATA5 expression in HCC cell lines, suppressing tumor cell growth and colony formation, as well as inducing apoptosis.

show abstract

Section: A B C D Ementioning

confidence: 72%

Loss of GATA5 expression due to gene promoter methylation induces growth and colony formation of hepatocellular carcinoma cells

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Combination treatment of TSA and cisplatin showed better efficacy than single drugs and significantly suppressed cell viability, migration, and spheroid formation and growth in human ovarian cancer cells. 51 The combined treatment of TSA and cisplatin synergistically inhibited cell proliferation, induced apoptosis, and increased the inhibition rate via significant decrease of cFLIP expression and increase of caspase-8 in A549 cells. 55 Similarly, TSA combined with palladium nanoparticles (PdNPs) showed an excellent synergistic effect on apoptosis in human cervical cancer cells.…”

Section: Combination Effect Of Rgo-ag and Tsa On Cell Viability And Cmentioning

confidence: 93%

“…50 Meng et al found that TSA inhibits the cell viability of SKOV3 in a dosedependent manner. 51 In another study, rheumatoid arthritis fibroblasts (RA-FLSs) like synoviocytes were subjected to hypoxia for 24 h in the presence or absence of 2 µM TSA and tested for cell viability, apoptosis, invasion, and gene expression. The results from this study suggested that TSA at a concentration up to 2 µM did not affect the viability of normal FLSs, and similarly, the hypoxic exposure did not affect the viability and apoptosis of RA-FLSs after 48-h incubation.…”

mentioning

confidence: 99%

Novel biomolecule lycopene-reduced graphene oxide-silver nanoparticle enhances apoptotic potential of trichostatin A in human ovarian cancer cells (SKOV3)

Zhang¹,

Huang²,

Zhang³

et al. 2017

IJN

View full text Add to dashboard Cite

Background Recently, there has been much interest in the field of nanomedicine to improve prevention, diagnosis, and treatment. Combination therapy seems to be most effective when two different molecules that work by different mechanisms are combined at low dose, thereby decreasing the possibility of drug resistance and occurrence of unbearable side effects. Based on this consideration, the study was designed to investigate the combination effect of reduced graphene oxide-silver nanoparticles (rGO-AgNPs) and trichostatin A (TSA) in human ovarian cancer cells (SKOV3). Methods The rGO-AgNPs were synthesized using a biomolecule called lycopene, and the resultant product was characterized by various analytical techniques. The combination effect of rGO-Ag and TSA was investigated in SKOV3 cells using various cellular assays such as cell viability, cytotoxicity, and immunofluorescence analysis. Results AgNPs were uniformly distributed on the surface of graphene sheet with an average size between 10 and 50 nm. rGO-Ag and TSA were found to inhibit cell viability in a dose-dependent manner. The combination of rGO-Ag and TSA at low concentration showed a significant effect on cell viability, and increased cytotoxicity by increasing the level of malondialdehyde and decreasing the level of glutathione, and also causing mitochondrial dysfunction. Furthermore, the combination of rGO-Ag and TSA had a more pronounced effect on DNA fragmentation and double-strand breaks, and eventually induced apoptosis. Conclusion This study is the first to report that the combination of rGO-Ag and TSA can cause potential cytotoxicity and also induce significantly greater cell death compared to either rGO-Ag alone or TSA alone in SKOV3 cells by various mechanisms including reactive oxygen species generation, mitochondrial dysfunction, and DNA damage. Therefore, this combination chemotherapy could be possibly used in advanced cancers that are not suitable for radiation therapy or surgical treatment and facilitate overcoming tumor resistance and disease progression.

show abstract

“…Cisplatin is used in combination with other chemical agents or compounds to treat ovarian cancer in both the resistant and sensitive cell lines. For example Cisplatin is used along with honey venom (Alizadehnohi, Nabiuni et al, 2012), withaferin (Kakar, Jala et al, 2012), trichostatin A or 5-aza-2′-deoxycytidine (Meng, Sun et al, 2013), overcoming chemotherapy resistance of ovarian cancer cells by liposomal Cisplatin (Koch, Krieger et al, 2013)…”

Section: Uses Of Cisplatin For Cancer Treatmentmentioning

confidence: 99%

Cisplatin in cancer therapy: Molecular mechanisms of action

Dasari

Tchounwou

2014

European Journal of Pharmacology

4,183

3,178

View full text Add to dashboard Cite

Cisplatin, cisplatinum, or cis-diamminedichloroplatinum (II), is a well-known chemotherapeutic drug. It has been used for treatment of numerous human cancers including bladder, head and neck, lung, ovarian, and testicular cancers. It is effective against various types of cancers, including carcinomas, germ cell tumors, lymphomas, and sarcomas. Its mode of action has been linked to its ability to crosslink with the purine bases on the DNA; interfering with DNA repair mechanisms, causing DNA damage, and subsequently inducing apoptosis in cancer cells. However, because of drug resistance and numerous undesirable side effects such as severe kidney problems, allergic reactions, decrease immunity to infections, gastrointestinal disorders, hemorrhage, and hearing loss especially in younger patients, other platinum-containing anti-cancer drugs such as carboplatin, oxaliplatin and others, have also been used. Furthermore, combination therapies of cisplatin with other drugs have been highly considered to overcome drug-resistance and reduce toxicity. This comprehensive review highlights the physicochemical properties of cisplatin and related platinum-based drugs, and discusses its uses (either alone or in combination with other drugs) for the treatment of various human cancers. A special attention is given to its molecular mechanisms of action, and its undesirable side effects.

show abstract

Anticancer efficacy of cisplatin and trichostatin A or 5-aza-2′-deoxycytidine on ovarian cancer

Cited by 60 publications

References 37 publications

Loss of GATA5 expression due to gene promoter methylation induces growth and colony formation of hepatocellular carcinoma cells

Loss of GATA5 expression due to gene promoter methylation induces growth and colony formation of hepatocellular carcinoma cells

Novel biomolecule lycopene-reduced graphene oxide-silver nanoparticle enhances apoptotic potential of trichostatin A in human ovarian cancer cells (SKOV3)

Cisplatin in cancer therapy: Molecular mechanisms of action

Contact Info

Product

Resources

About