Epigenetic Changes within the Promoter Regions of Antigen Processing Machinery Family Genes in Kazakh Primary Esophageal Squamous Cell Carcinoma

Sheyhidin, Ilyar; Hasim, Ayshamgul; Zheng, Feng; Ma, Hong

doi:10.7314/apjcp.2014.15.23.10299

Cited by 9 publications

(5 citation statements)

References 29 publications

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“…Recent studies have begun to determine the level of methylation at each CpG in the HLA gene loci in a variety of tumors (41,42). Using pyrosequencing, we quantified methylation at all the CpG sites individually in the HLA-A3 proximal promoter in COPA-159 cells and found that they were not equally susceptible to demethylation treatment; specifically, those close to site-␣ and the TATA box were demethylated to a greater extent than other sites.…”

Section: Discussionmentioning

confidence: 99%

Multiple Structural and Epigenetic Defects in the Human Leukocyte Antigen Class I Antigen Presentation Pathway in a Recurrent Metastatic Melanoma Following Immunotherapy

Chang

Pirozzi²,

Wen

et al. 2015

Journal of Biological Chemistry

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Background: Understanding the mechanism of tumor immune resistance can help design effective cancer immunotherapy. Results: A novel tapasin mutation, haplotype loss, and HLA epigenetic repression were identified and characterized in a single tumor population. Conclusion:The first evidence for combined HLA genetic and epigenetic defects in malignant cells was presented. Significance: Combinatorial immunotherapy harnessing T cell responses and DNA demethylation may counteract tumor immune resistance.

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Section: Discussionmentioning

confidence: 99%

Multiple Structural and Epigenetic Defects in the Human Leukocyte Antigen Class I Antigen Presentation Pathway in a Recurrent Metastatic Melanoma Following Immunotherapy

Chang

Pirozzi²,

Wen

et al. 2015

Journal of Biological Chemistry

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“…This vaccine could induce both therapeutic and protective antitumor immune responses. It has been reported that HDACi can regulate the expression levels of numerous genes (26,30), which is considered as an additional mechanism rather than direct presentation.…”

Section: Discussionmentioning

confidence: 99%

Trichostatin A-modified vaccine provides superior protection against ovarian cancer formation and development

Liu,

Yi,

Meng

et al. 2024

Braz J Med Biol Res

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More attention has been paid to immunotherapy for ovarian cancer and the development of tumor vaccines. We developed a trichostatin A (TSA)-modified tumor vaccine with potent immunomodulating activities that can inhibit the growth of ovarian cancer in rats and stimulate immune cell response in vivo. TSA-treated Nutu-19 cells inactivated by X-ray radiation were used as a tumor vaccine in rat ovarian cancer models. Prophylactic and therapeutic experiments were performed with TSA-modified tumor vaccine in rats. Flow cytometry and ELISpot assays were conducted to assess immune response. Immune cell expression in the spleen and thymus were detected by immunohistochemical staining. GM-CSF, IL-7, IL-17, LIF, LIX, KC, MCP-1, MIP-2, M-CSF, IP-10/CXCL10, MIG/CXCL9, RANTES, IL-4, IFN-g, and VEGF expressions were detected with Milliplex Map Magnetic Bead Panel immunoassay. TSA vaccination in therapeutic and prophylactic models could effectively stimulate innate immunity and boost the adaptive humoral and cell-mediated immune responses to inhibit the growth and tumorigenesis of ovarian cancer. This vaccine stimulated the thymus into reactivating status and enhanced infiltrating lymphocytes in tumorbearing rats. The expression of key immunoregulatory factors were upregulated in the vaccine group. The intensities of infiltrating CD4+ and CD8+ T cells and NK cells were significantly increased in the vaccine group compared to the control group (Po0.05). This protection was mainly dependent on the IFN-g pathway and, to a much lesser extent, by the IL-4 pathway. The tumor cells only irradiated by X-ray as the control group still showed a slight immune effect, indicating that irradiated cells may also cause certain immune antigen exposure, but the efficacy was not as significant as that of the TSA-modified tumor vaccine. Our study revealed the potential application of the TSA-modified tumor vaccine as a novel tumor vaccine against tumor refractoriness and growth. These findings offer a better understanding of the immunomodulatory effects of the vaccine against latent tumorigenesis and progression. This tumor vaccine therapy may increase antigen exposure, synergistically activate the immune system, and ultimately improve remission rates. A vaccine strategy designed to induce effective tumor immune response is being considered for cancer immunotherapy.

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“…In the case of MHC-I genes, downregulation of HLA-A and β2M has been previously linked to esophageal carcinoma pathogenesis, while overexpression of microRNAs, miR-148a-3p and miR-125a-5p, has been associated with downregulation of MHC-I genes, such as TAP2, in this type of malignancies [ 85 ]. Moreover, multiple CpG sites were linked to loss of HLA-B and other associated genes, such as TAP2 and LMP7 [ 86 ]. However, human tissue microarrays indicated that patients with head and neck cancer exhibited heterogenous expression of HLA-DRB and LMP7 proteins (Fig.…”

Section: Esophageal Cancer and Immunoepigenetic De...mentioning

confidence: 99%

“…However, human tissue microarrays indicated that patients with head and neck cancer exhibited heterogenous expression of HLA-DRB and LMP7 proteins (Fig. 7 a, c), and the corresponding gene expression changes did not predict a significant difference in survival probability [ 86 ]. (Fig.…”

Section: Esophageal Cancer and Immunoepigenetic De...mentioning

confidence: 99%

Epigenetic regulation of major histocompatibility complexes in gastrointestinal malignancies and the potential for clinical interception

Tovar Perez,

Zhang,

Hodgeman

et al. 2024

Clin Epigenet

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Background Gastrointestinal malignancies encompass a diverse group of cancers that pose significant challenges to global health. The major histocompatibility complex (MHC) plays a pivotal role in immune surveillance, orchestrating the recognition and elimination of tumor cells by the immune system. However, the intricate regulation of MHC gene expression is susceptible to dynamic epigenetic modification, which can influence functionality and pathological outcomes. Main body By understanding the epigenetic alterations that drive MHC downregulation, insights are gained into the molecular mechanisms underlying immune escape, tumor progression, and immunotherapy resistance. This systematic review examines the current literature on epigenetic mechanisms that contribute to MHC deregulation in esophageal, gastric, pancreatic, hepatic and colorectal malignancies. Potential clinical implications are discussed of targeting aberrant epigenetic modifications to restore MHC expression and 0 the effectiveness of immunotherapeutic interventions. Conclusion The integration of epigenetic-targeted therapies with immunotherapies holds great potential for improving clinical outcomes in patients with gastrointestinal malignancies and represents a compelling avenue for future research and therapeutic development.

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Epigenetic Changes within the Promoter Regions of Antigen Processing Machinery Family Genes in Kazakh Primary Esophageal Squamous Cell Carcinoma

Cited by 9 publications

References 29 publications

Multiple Structural and Epigenetic Defects in the Human Leukocyte Antigen Class I Antigen Presentation Pathway in a Recurrent Metastatic Melanoma Following Immunotherapy

Multiple Structural and Epigenetic Defects in the Human Leukocyte Antigen Class I Antigen Presentation Pathway in a Recurrent Metastatic Melanoma Following Immunotherapy

Trichostatin A-modified vaccine provides superior protection against ovarian cancer formation and development

Epigenetic regulation of major histocompatibility complexes in gastrointestinal malignancies and the potential for clinical interception

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