Histone deacetylase inhibitors enhance oncolytic herpes simplex virus therapy for malignant meningioma

Kawamura, Yoichiro; Hua, Lingyang; Gurtner, Alessandra; Wong, Ego; Kiyokawa, Juri; Shah, Nusrat; Gorham, Joshua M.; Wakimoto, Hiroko; Rabkin, Samuel D.; Martuza, Robert L.; Wakimoto, Hiroaki

doi:10.1016/j.biopha.2022.113843

Cited by 6 publications

(8 citation statements)

References 50 publications

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“…The use of OVs with or without combinatorial drugs or radiotherapy has been taken to the clinic as a potential future treatment modality for TNBC and many other cancer types. Combinatorial regimens, such as the use of HDACis to enhance oncolytic HSV entry and replication within tumor cells [ 182 ], show that new pairings of already-existing therapies with OVs can lead to promising outcomes that can be translated quickly into human trials. Immuno-oncolytic viruses and other immunotherapies reflect a shift from a chemical to biological approach in the treatment of cancers.…”

Section: Discussionmentioning

confidence: 99%

Triple-Negative Breast Cancer: Basic Biology and Immuno-Oncolytic Viruses

Monaco

Idris

Essani

2023

Cancers

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Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer. TNBC diagnoses account for approximately one-fifth of all breast cancer cases globally. The lack of receptors for estrogen, progesterone, and human epidermal growth factor 2 (HER-2, CD340) results in a lack of available molecular-based therapeutics. This increases the difficulty of treatment and leaves more traditional as well as toxic therapies as the only available standards of care in many cases. Recurrence is an additional serious problem, contributing substantially to its higher mortality rate as compared to other breast cancers. Tumor heterogeneity also poses a large obstacle to treatment approaches. No driver of tumor development has been identified for TNBC, and large variations in mutational burden between tumors have been described previously. Here, we describe the biology of six different subtypes of TNBC, based on differential gene expression. Subtype differences can have a large impact on metastatic potential and resistance to treatment. Emerging antibody-based therapeutics, such as immune checkpoint inhibitors, have available targets for small subsets of TNBC patients, leading to partial responses and relatively low overall efficacy. Immuno-oncolytic viruses (OVs) have recently become significant in the pursuit of effective treatments for TNBC. OVs generally share the ability to ignore the heterogeneous nature of TNBC cells and allow infection throughout a treated tumor. Recent genetic engineering has allowed for the enhancement of efficacy against certain tumor types while avoiding the most common side effects in non-cancerous tissues. In this review, TNBC is described in order to address the challenges it presents to potential treatments. The OVs currently described preclinically and in various stages of clinical trials are also summarized, as are their strategies to enhance therapeutic potential.

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Section: Discussionmentioning

confidence: 99%

Triple-Negative Breast Cancer: Basic Biology and Immuno-Oncolytic Viruses

Monaco

Idris

Essani

2023

Cancers

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“…HDAC inhibition assists multiple processes of oncolytic virotherapy, such as enhancing virus entry, replication, propagation, and spread; decreasing antivirus response; promoting apoptosis; and induction of tumor antigen expression 27,28 . Among several HDAC inhibitors, TSA, the pan‐HDAC inhibitor, targets class I (HDAC1, HDAC2, HDAC3, and HDAC8) and class II (HDAC4, HDAC5, HDAC6, HDAC7, HDAC9, and HDAC10) HDACs and is frequently combined with several OVs, such as adenovirus, 32–36 bovine herpesvirus type 1, 37 and herpes simplex virus 38–40 . It is also the most potent enhancer of VV replication and spread among other HDAC inhibitors 26 …”

Section: Discussionmentioning

confidence: 99%

“…TSA activated viral replication in CT26 cells in an antivirus IFN‐independent manner. Suppression of the IFN‐mediated antivirus response by TSA depends on the cell context, as reported previously 39 . This might explain why both virus spread and cytotoxicity of non‐fusogenic MDRVV were observed only in B16‐F10 cells.…”

Section: Discussionmentioning

confidence: 99%

“…27,28 Among several HDAC inhibitors, TSA, the pan-HDAC inhibitor, targets class I (HDAC1, HDAC2, HDAC3, and HDAC8) and class II (HDAC4, HDAC5, HDAC6, HDAC7, HDAC9, and HDAC10) HDACs and is frequently combined with several OVs, such as adenovirus, [32][33][34][35][36] bovine herpesvirus type 1, 37 and herpes simplex virus. [38][39][40] It is also the most potent enhancer of VV replication and spread among other HDAC inhibitors. 26 B16-F10 melanoma cells, which were previously used in combination with non-fusogenic VV (TK-B18R-) and TSA, 26 showed smaller cell-cell fusion formation with FUVAC treatment.…”

Section: Discussionmentioning

confidence: 99%

“… 27 , 28 Among several HDAC inhibitors, TSA, the pan‐HDAC inhibitor, targets class I (HDAC1, HDAC2, HDAC3, and HDAC8) and class II (HDAC4, HDAC5, HDAC6, HDAC7, HDAC9, and HDAC10) HDACs and is frequently combined with several OVs, such as adenovirus, 32 , 33 , 34 , 35 , 36 bovine herpesvirus type 1, 37 and herpes simplex virus. 38 , 39 , 40 It is also the most potent enhancer of VV replication and spread among other HDAC inhibitors. 26 …”

Section: Discussionmentioning

confidence: 99%

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Histone deacetylase inhibitor boosts anticancer potential of fusogenic oncolytic vaccinia virus by enhancing cell–cell fusion

Nakatake,

Kurosaki,

Nakamura

2023

Cancer Science

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Oncolytic viruses have two anticancer functions: direct oncolysis and elicitation of antitumor immunity. We previously developed a novel fusogenic oncolytic vaccinia virus (FUVAC) from a non‐fusogenic vaccinia virus (VV) and, by remodeling the tumor immune microenvironment, we demonstrated that FUVAC induced stronger oncolysis and antitumor immune responses compared with non‐fusogenic VV. These functions depend strongly on cell–cell fusion induction. However, FUVAC tends to have decreased fusion activity in cells with low virus replication efficacy. Therefore, another combination strategy was required to increase cell–cell fusion in these cells. Histone deacetylase (HDAC) inhibitors suppress the host virus defense response and promote viral replication. Therefore, in this study, we selected an HDAC inhibitor, trichostatin A (TSA), as the combination agent for FUVAC to enhance its fusion‐based antitumor potential. TSA was added prior to FUVAC treatment of murine tumor B16‐F10 and CT26 cells. TSA increased the replication of both FUVAC and parental non‐fusogenic VV. Moreover, TSA enhanced cell–cell fusion and FUVAC cytotoxicity in these tumor cells in a dose‐dependent manner. Transcriptome analysis revealed that TSA‐treated tumors showed altered expression of cellular component‐related genes, which may affect fusion tolerance. In a bilateral tumor‐bearing mouse model, combination treatment of TSA and FUVAC significantly prolonged mouse survival compared with either treatment alone or in combination with non‐fusogenic VV. Our findings demonstrate that TSA is a potent enhancer of cell–cell fusion efficacy of FUVAC.

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Advances in antitumour therapy with oncolytic herpes simplex virus combinations

2024

Discov Onc

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Oncolytic Virus (OVs) is an emerging approach to tumour immunity that allows the use of natural or genetically modified viruses to specifically infect and lyse tumour cells without damaging normal cells. Oncolytic herpes simplex virus (oHSV) is one of the more widely researched and applied OVs in the field of oncology, which can directly kill tumour cells to promote anti-tumour immune responses. oHSV is one of the few viruses with good antiviral drugs, so oHSV is also more clinically safe. In recent years, in addition to monotherapy of oHSV in tumours, more and more studies have been devoted to exploring the anti-tumour effects of oHSV in combination with other therapeutic approaches. In this article we describe the progress of oHSV combination therapy against tumours in the nervous system, digestive system, reproductive system and other systems.

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Histone deacetylase inhibitors enhance oncolytic herpes simplex virus therapy for malignant meningioma

Cited by 6 publications

References 50 publications

Triple-Negative Breast Cancer: Basic Biology and Immuno-Oncolytic Viruses

Triple-Negative Breast Cancer: Basic Biology and Immuno-Oncolytic Viruses

Histone deacetylase inhibitor boosts anticancer potential of fusogenic oncolytic vaccinia virus by enhancing cell–cell fusion

Advances in antitumour therapy with oncolytic herpes simplex virus combinations

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