Potentiation of anticancer effect of valproic acid, an antiepileptic agent with histone deacetylase inhibitory activity, by the cyclin-dependent kinase inhibitor P276-00 in human non-small-cell lung cancer cell lines

Shirsath, Nitesh; Rathos, Maggie J.; Chaudhari, Umesh; Sivaramakrishnan, H.; Joshi, Kalpana

doi:10.1016/j.lungcan.2013.08.010

Cited by 20 publications

(15 citation statements)

References 27 publications

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“…Figure 5 shows 35% and 41% compared to treated with only HG-MNS-DOX (13%) without any RF exposure. In these cases, the RF treatment induced a strong G1 phase arrest due to inhibition in DNA replication which eventually leads to cells apoptosis [32], [33]. These results suggest that the drug loaded MNS improves efficacy of cell apoptosis by combined therapy which can lead to a better therapeutic outcome in future.…”

Section: Cell Cycle Analysis and Apoptotic Populationmentioning

confidence: 86%

Magneto-thermally responsive hydrogels for bladder cancer treatment: Therapeutic efficacy and in vivo biodistribution

Jaiswal

Pradhan

Vasavada

et al. 2015

Colloids and Surfaces B: Biointerfaces

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Section: Cell Cycle Analysis and Apoptotic Populationmentioning

confidence: 86%

Magneto-thermally responsive hydrogels for bladder cancer treatment: Therapeutic efficacy and in vivo biodistribution

Jaiswal

Pradhan

Vasavada

et al. 2015

Colloids and Surfaces B: Biointerfaces

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“…However, the HDAC inhibitory mechanism of VPA is relatively well known. [8][9][10] HDAC is reported to be aberrantly expressed in diverse cancers. HDAC inhibition can increase the expression of several genes by accelerating their transcription, which can enhance the innate immune system and lead to suppression of tumor growth.…”

Section: Discussionmentioning

confidence: 99%

“…However, a synergistic effect of VPA with other agents has been reported in some promising results. [8][9][10] VPA upregulates MIC-A and MIC-B, 11 and this upregulation on the tumor surface enhances CIK cells effects. Moreover, VPA has been safely used as an antiepileptic drug for decades, it is relatively inexpensive, and its adverse effects have been regarded as tolerable.…”

Section: Introductionmentioning

confidence: 97%

Synergistic effect of cytokine-induced killer cell with valproate inhibits growth of hepatocellular carcinoma cell in a mouse model

Lee

Nam

Chang

et al. 2017

Cancer Biology & Therapy

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Objective: Long-term prognosis of hepatocellular carcinoma (HCC) remains poor owing to the lack of treatment options for advanced HCC. Cytokine-induced killer (CIK) cells are ex vivo expanded T lymphocytes expressing both NK-and T-cell markers. CIK cell therapy alone is insufficient for treating advanced HCC. Thus, this study aimed to determine whether treatment with CIK cells combined with valproic acid (VPA) could provide a synergistic effect to inhibit tumor growth in a mouse model of HCC. Methods: Upregulation of natural killer group 2D (NKG2D) ligands (retinoic acid early inducible 1 [RAE-1], mouse; major histocompatibility complex class I polypeptide-related sequence A [MIC-A], human) were evaluated by FACS. VPA concentrations that did not reduce tumor volume were calculated to avoid VPA cytotoxicity in a C3H mouse model of HCC. CIK cells were generated from mouse splenocytes using interferon gamma, a CD3 monoclonal antibody, and interleukin 2. The potential synergistic effect of CIK cells combined with VPA was evaluated in the mouse model and tissue pathology was investigated. Results: After 40 h of incubation with VPA, RAE-1 and MIC-A expression were increased in 4 HCC cell lines compared with that in control (2.3-fold in MH-134, 2.4-fold in Huh-7, 3.7-fold in SNU-761, and 6.5-fold in SNU-475). The maximal in vivo VPA dosage that showed no significant cytotoxicity compared with control was 10 mg/kg/day. CIK cells were well generated from C3H mouse splenocytes. After 7 d of treatment with CIK cells plus VPA, a synergistic effect was observed on relative tumor volume in the mouse model of HCC. While the relative tumor volume in untreated control mice increased to 11.25, that in the combination treatment group increased to only 5.20 (P D 0.047). Conclusions: The VPA-induced increase in NKG2D ligands expression significantly enhanced the effects of CIK cell therapy in a mouse model of HCC.

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“…A lot of study has been done on the effects of valproic acid on the growth of cancer cells such as glioblastoma and ovarian cancer cells. The anti cancer properties exhibited by valproic acid is linked to its ability to inhibit histone deacetylase and also to act independently of hormones and other mechanisms such as multidrug protein resistance [5].…”

Section: Anti Epileptic Medicines and How They Stop Or Slow Down Tumomentioning

confidence: 99%

A New Theoretical Approach for Cancer Prevention: A Novel Strategy of using Anti-Epileptic Medicines to Prevent Tumour Growth

Pehlıvan

2017

JACCOA

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Potentiation of anticancer effect of valproic acid, an antiepileptic agent with histone deacetylase inhibitory activity, by the cyclin-dependent kinase inhibitor P276-00 in human non-small-cell lung cancer cell lines

Cited by 20 publications

References 27 publications

Magneto-thermally responsive hydrogels for bladder cancer treatment: Therapeutic efficacy and in vivo biodistribution

Magneto-thermally responsive hydrogels for bladder cancer treatment: Therapeutic efficacy and in vivo biodistribution

Synergistic effect of cytokine-induced killer cell with valproate inhibits growth of hepatocellular carcinoma cell in a mouse model

A New Theoretical Approach for Cancer Prevention: A Novel Strategy of using Anti-Epileptic Medicines to Prevent Tumour Growth

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