• IMMUNE NETWORK
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• v.9 no.4
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• pp.122-126
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• 2009

Transforming growth factor-$\beta$ (TGF-$\beta$) is a highly pleiotropic cytokine playing pivotal roles in immune regulation. TGF-$\beta$ facilitates tumor cell survival and metastasis by targeting multiple cellular components. Focusing on its immunosuppressive functions, TGF-$\beta$ antagonists have been employed for cancer treatment to enhance tumor immunity. TGF-$\beta$ antagonists exert anti-tumor effects through #1 activating effector cells such as NK cells and cytotoxic $CD8^+$ Tcells (CTLs), #2 inhibiting regulatory/suppressor cell populations, #3 making tumor cells visible to immune cells, #4 inhibiting the production of tumor growth factors. This review focuses on the effect of TGF-$\beta$ on T cells, which are differentiated into effector T cells or newly identified tumor-supporting T cells.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.2
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• pp.389-397
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• 2005

This experimental Study was designed to investigate the effects of Acanthopanacis Cortex Extract(ACE) on the immunity, anti-cancer and obesity in mice. The results were as follows; ACE was significantly increased in the proliferation of thymocytes and splenocytes, and NO production from peritoneal macrophages in normal mice. ACE was significantly increased in the proliferation of thymocytes and splenocytes, and NO production from peritoneal macrophages in L1210 cells transplanted mice. ACE was significantly decreased in the proliferation of L1210 cells in L1210 cells transplanted mice. ACE was significantly inhibited body weight and tumor weight in S-180 cells transplanted mice. ACE was significantly increased in the mean survival days in S-180 cells transplanted mice. ACE was significantly decreased in the body weight in rats fed high fat diet. ACE was significantly decreased in the serum total cholesterol level, free fatty acid level, total lipid level, phospholipid level in rats fed high fat diet. According to above results, the authors suggest that ACE is able to be used for the herb of physiological-action.

• BMB Reports
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• v.56 no.11
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• pp.584-593
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• 2023

Hypoxia, a widespread occurrence observed in various malignant tumors, results from rapid tumor growth that outpaces the oxygen supply. Tumor hypoxia precipitates several effects on tumor biology; these include activating angiogenesis, intensifying invasiveness, enhancing the survival of tumor cells, suppressing anti-tumor immunity, and fostering resistance to therapy. Aligned with the findings that correlate CMGC kinases with the regulation of Hypoxia-Inducible Factor (HIF), a pivotal modulator, reports also indicate that hypoxia governs the activity of CMGC kinases, including DYRK1 kinases. Prolyl hydroxylation of DYRK1 kinases by PHD1 constitutes a novel mechanism of kinase maturation and activation. This modification "primes" DYRK1 kinases for subsequent tyrosine autophosphorylation, a vital step in their activation cascade. This mechanism adds a layer of intricacy to comprehending the regulation of CMGC kinases, and underscores the complex interplay between distinct post-translational modifications in harmonizing precise kinase activity. Overall, hypoxia assumes a substantial role in cancer progression, influencing diverse aspects of tumor biology that include angiogenesis, invasiveness, cell survival, and resistance to treatment. CMGC kinases are deeply entwined in its regulation. To fathom the molecular mechanisms underpinning hypoxia's impact on cancer cells, comprehending how hypoxia and prolyl hydroxylation govern the activity of CMGC kinases, including DYRK1 kinases, becomes imperative. This insight may pave the way for pioneering therapeutic approaches that target the hypoxic tumor microenvironment and its associated challenges.

• Proceedings of the Zoological Society Korea Conference
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• 2001.10a
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• pp.261.2-261
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• 2001

No Abstract, See Full Text

• Proceedings of the Microbiological Society of Korea Conference
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• 2007.05a
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• pp.94-94
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• 2007

• CELLMED
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• v.3 no.1
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• pp.3.1-3.3
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• 2013

The receptor activator of NF-${\kappa}B$ ligand (RANKL), a member of the tumor necrosis factor ligand family, has extensive functions beyond osteoclast development. RANKL is expressed in many immune cells such as osteoblasts, osteocytes, marrow stromal cells, activated T cells, synovial cells, keratinocytes, and mammary gland epithelial cells as well as in various tissues. The ligation of RANK by RANKL promotes dendritic cells (DCs) survival through prosurvival signals and the up-regulation of the anti-apoptotic proteins Bcl-2 and Bcl-$x_L$ and plays a crucial role in DCs-mediated Th1 differentiation. Therefore, RANKL plays an important role in the regulation of DCs/T cells-mediated specific immunity. This review will briefly inform our current understanding of the role of RANKL signaling in T cells-DCs communication in the immune system.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.5
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• pp.3109-3116
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• 2013

The majority of hepatocellular carcinoma (HCC) patients have a poor prognosis with current therapies, and new approaches are urgently needed. We have developed a novel therapeutic cancer vaccine platform based on tumor cell derived autophagosomes (DRibbles) for cancer immunotherapy. We here evaluated the effectiveness of DRibbles-pulsed dendritic cell (DC) immunization to induce anti-tumor immunity in BALB/c mouse HCC and humanized HCC mouse models generated by transplantation of human HCC cells (HepG2) into BALB/c-nu mice. DRibbles were enriched from H22 or BNL cells, BALB/c-derived HCC cell lines, by inducing autophagy and blocking protein degradation. DRibbles-pulsed DC immunization induced a specific T cell response against HCC and resulted in significant inhibition of tumor growth compared to mice treated with DCs alone. Antitumor efficacy of the DCs-DRibbles vaccine was also demonstrated in a humanized HCC mouse model. The results indicated that HCC/DRibbles-pulsed DCs immunotherapy might be useful for suppressing the growth of residual tumors after primary therapy of human HCC.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.8
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• pp.3829-3833
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• 2016

Inhibition of cancer-associated fibroblasts (CAFs) may improve the efficacy of cancer therapy. Polysaccharide extracted from polygonatum can selectively inhibit the growth of prostate-CAFs (p<0.001) without inhibiting the growth of normal fibroblasts (NAFs). Polysaccharides from polygonatum stimulate autophagy of prostate-CAFs. 3-methyl-adenine(3-MA) is an autophagy inhibitor. 3-MA was added to prostate-CAFs with polysaccharide from polygonatum to determine whether autophagy plays an important role in the restrained effect. Finally, polysaccharide from polygonatum treatment significantly increased the activation of Beclin-1 and LC3, key autophagy proteins. Polysaccharide from polygonatum stimulates autophagy of prostate-CAFs and inhibits prostate-CAF growth, indicating that a novel anti-cancer strategy involves inhibiting the growth of prostate-CAFs.

• Journal of Life Science
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• v.29 no.7
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• pp.824-835
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• 2019

In recent decades, oncolytic viruses (OVs) have extensively been investigated as a potential cancer drug. Oncolytic viruses have primarily the unique advantage in the fact that they can only infect and destroy cancer cells. Secondary, oncolytic viruses induce the activation of specific adaptive immunity which targets tumor-associated antigens that were hidden during the initial cancer progression. In 2015, one genetically modified oncolytic virus, talimogene laherparepvec (T-VEC), was approved by the American Food and Drug Administration (FDA) for the treatment of melanoma. Currently, various oncolytic viruses are being investigated in clinical trials as monotherapy or in combination with preexistent cancer therapies like immunotherapy, radiotherapy or chemotherapy. The efficacy of oncolytic virotherapy relies on the balance between the induced anti-tumor immunity and the anti-viral response. Despite the revolutionary outcome, the development of oncolytic viruses for the treatment of cancer faces a number of obstacles such as delivery method, neutralizing antibodies and induction of antiviral immunity due to the complexity, variability and reactivity of tumors. Intratumoral administration has been successful reducing considerably solid tumors with no notable side effects unfortunately some tumors are not accessible (brain) and require a systemic administration of the oncolytic viruses. In order to overcome these hurdles, various strategies to enhance the efficacy of oncolytic viruses have been developed which include the insertion of transgenes or combination with immune-modulatory substances.

• The Journal of Korean Medicine
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• v.27 no.4
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• pp.12-29
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• 2006

Background and Aims : Even though various strategies for cancer treatment have advanced with the remarkable development of genomic information and technology, it is far from giving relief to cancer patients. Recently there is accumulating evidence that the immune system is closely connected to anti-tumor defense mechanisms in a multistage process. This includes tumorigenesis, invasion, growth and metastasis. Cordyceps Militaris, a well-known oriental herbal medicine, is a parasitic fungus that has been used as an immune enhancing agent for a long period of time. However, little is known about the cancer-related immunomodulatory effects and anti-tumor activities. In the present study, we aimed to investigate the effects of Cordyceps Militaris extract (CME) on immune modulating and anti-tumor activity. Materials and Methods : To elucidate the effects of CME on macrophage and natural killer (NK) cell activity, we analyzed nitric oxide (NO) production, NK cytotoxicity and gene expression of cytokines related with macrophages and NK cell activity. Results and Conclusions : CME activated and promoted macrophage production of NO. It also enhanced gene expression of IL-1 and iNOS in RAW 264.7 cells. CME promoted cytotoxicity of NK cells against YAC-1 cells and enhanced NK cell related gene expression such as IL-1, IL-2, IL-12, iNOS, IFN-${\gamma}$ and　TNF-${\alpha}$ in mice splenocytes. It also Promoted protein expression of IL-10, IL-12, IFN-${\gamma}$ and TNF-${\alpha}$ in mice splenocytes and inhibited lung tumor metastasis induced by CT-26 cell line compared with the control group. From these results, it could be concluded that CME is an effective herbal drug for modulating the immune system and anti-cancer treatment by promoting macrophage and NK cell activity.