Tumor-specific promoter-driven adenoviral therapy for insulinoma

Tseng, Alan; Chen, Chiachen; Breslin, Mary B.; Lan, Michael S.

doi:10.1007/s13402-016-0274-8

Cited by 15 publications

(5 citation statements)

References 12 publications

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“…Delivery vector is crucial to HSV-TK/GCV system. Some viral-mediated HSV-TK/GCV system limited it use for severe immune and inflammatory responses (Hall et al, 1997; Staquicini et al, 2020; Tseng et al, 2016). BF is a nonpathogenic, intrinsic and anaerobic bacterium, which selectively localizes and proliferates in the central area of solid tumors after administrated via the vein or intratumor injection.…”

Section: Discussionmentioning

confidence: 99%

Bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir treatment inhibits cancer metastasis

Wang

Shen

et al. 2022

Preprint

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Previous studies have found that Bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir (BF-TK/GCV) reduces the expression of VEGF and CD146 which implies tumor metastasis inhibition. However, the mechanism of BF-TK/GCV inhibits tumor metastasis is still not fully studied. Here, we comprehensively identified and quantified protein expression profiling for the first time in gastric cancer (GC) cells MKN-45 upon BF-TK/GCV treatment using quantitative proteomics. A total of 159 and 72 differential expression proteins (DEPs) were significantly changed in BF-TK/GCV / BF-TK and BF-TK/GCV / BF/GCV groups. Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis showed some enriched metastasis-related pathways such as gap junction and cell adhesion molecules pathways. Moreover, transwell assay proved that BF-TK/GCV inhibited the invasion and migration of tumor cells. Furthermore, immunohistochemistry (IHC) demonstrated that BF-TK/GCV reduced the expression of HIF-1A, MTOR, NF-?B1-p105, VCAM1, CEBPB and CXCL12, which were associated with tumor metastasis. In summary, besides apoptosis, BF-TK/GCV also inhibited tumor metastasis, which deepened and expanded the understanding of BF-TK/GCV anti-tumor mechanisms.

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Section: Discussionmentioning

confidence: 99%

Bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir treatment inhibits cancer metastasis

Wang

Shen

et al. 2022

Preprint

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“…No. 90111, Waltham, MA, USA) according to the manufacturer's instructions [75]. Then, the pooled samples were fractionated into fractions by ACQUITY Ultra Performance liquid chromatography (Waters, Milford, MA, USA) with ACQUITY UPLC BEH C18 Column (1.7 µm, 2.1 mm × 150 mm, Waters, Milford, MA, USA) to increase proteomic depth.…”

Section: Liquid Chromatography-tandem Mass Spectrometry (Lc-ms/ms) An...mentioning

confidence: 99%

Bifidobacterium infantis-Mediated Herpes Simplex Virus-TK/Ganciclovir Treatment Inhibits Cancer Metastasis in Mouse Model

Wang

Shen

2023

IJMS

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Previous studies have found that Bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir (BF-TK/GCV) reduces the expression of VEGF and CD146, implying tumor metastasis inhibition. However, the mechanism by which BF-TK/GCV inhibits tumor metastasis is not fully studied. Here, we comprehensively identified and quantified protein expression profiling for the first time in gastric cancer (GC) cells MKN−45 upon BF-TK/GCV treatment using quantitative proteomics. A total of 159 and 72 differential expression proteins (DEPs) were significantly changed in the BF-TK/GCV/BF-TK and BF-TK/GCV/BF/GCV comparative analysis. Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis enriched some metastasis-related pathways such as gap junction and cell adhesion molecules pathways. Moreover, the transwell assay proved that BF-TK/GCV inhibited the invasion and migration of tumor cells. Furthermore, immunohistochemistry (IHC) demonstrated that BF-TK/GCV reduced the expression of HIF−1α, mTOR, NF-κB1-p105, VCAM1, MMP13, CXCL12, ATG16, and CEBPB, which were associated with tumor metastasis. In summary, BF-TK/GCV inhibited tumor metastasis, which deepened and expanded the understanding of the antitumor mechanism of BF-TK/GCV.

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“…Important viral genes can also be placed under transcriptional control of cancer cell or tissue-specific promoters. This has been done with the Ad E1A protein, whereby placing it under control of an insulinoma-associated 1 promoter leads to specific replication in developing neuroendocrine pancreatic islet tumors [52] and likewise, in prostate cancer when under the control of prostatespecific antigen [53]. In HSV-1, this same effect has been achieved by placing the essential viral gene ICP4 under translational control of a glioma-specific survivin protein [54].…”

Section: Ovsmentioning

confidence: 99%

Oncolytic virus-induced cell death and immunity: a match made in heaven?

Munck

Binks

McNeish

et al. 2017

Journal of Leukocyte Biology

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Our understanding of the mechanisms responsible for cancer development has increased enormously over the last decades. However, for many cancers, this has not been translated into a significant improvement in overall survival, and overall mortality remains high. Treatment for many malignancies remains based on surgery, chemotherapy, and radiotherapy. Significant progress has been made toward the development of more specific, more potent, and less invasive treatment modalities, but such targeted therapies remain the exception for most cancers. Thus, cancer therapies based on a different mechanism of action should be explored. The immune system plays an important role in keeping tumor growth at bay. However, in many cases, these responses are not strong enough to keep tumor growth under control. Thus, immunotherapy aims to boost the immune system to suppress tumor growth efficiently. This has been demonstrated by the recent successes of immune checkpoint therapy in several cancers. Oncolytic viruses (OVs) are another exciting class of immunotherapy agent. As well as replicating selectively within and killing tumor cells, OVs are able to elicit potent anti-tumor immune responses. Therapeutic vaccination with OVs, also referred to as cancer virotherapy, can thus be tailored to elicit vigorous cellular immune responses and even target individual malignancies in a personalized manner. In this review, we will describe the intricate link among oncolytic virotherapy, tumor immunology, and immunogenic cell death (ICD) and discuss ways to harness optimally their potential for future cancer therapy.

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Tumor-specific promoter-driven adenoviral therapy for insulinoma

Abstract: INSM1 promoter-driven conditionally replicating adenoviruses may serve as a new tool for the treatment of insulinoma and may provide clinicians with additional options to combat this disease.

Cited by 15 publications

References 12 publications

Bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir treatment inhibits cancer metastasis

Bifidobacterium infantis-mediated herpes simplex virus-TK/ganciclovir treatment inhibits cancer metastasis

Bifidobacterium infantis-Mediated Herpes Simplex Virus-TK/Ganciclovir Treatment Inhibits Cancer Metastasis in Mouse Model

Oncolytic virus-induced cell death and immunity: a match made in heaven?

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