• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3569-3572
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• 2012

Social support is regarded as a complex construct which has long been suggested to have direct and buffering effects on patients' wellbeing and emotional adjustment to cancer. Cross-sectional and prospective studies show a positive association between perceived social support and psychological adjustment following cancer treatment. Research findings suggest that the evidence for the relationship between social support and cancer progression is sufficiently strong. This report points out the importance of social support in cancer and provides recommendations for health care professionals.

• Journal of Gastric Cancer
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• v.14 no.2
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• pp.123-128
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• 2014

Purpose: Since there are no proven tumor markers that reflect the course of gastric cancer, carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) are commonly used alternatives. However, the degree of progression that corresponds to an increase in these markers, and the values of these markers at different cancer stages, remains unclear. Materials and Methods: This study enrolled 1,733 gastric cancer patients who underwent surgery and whose pre-operative CEA and CA19-9 levels were known. Survival curves and mean values of the two markers were compared according to the degree of cancer progression: serosa-unexposed (SU), serosa-exposed (SE), direct invasion (DI), localized seeding (P1), and extensive seeding (P2). Results: The 5-year overall survival rates at each stage differed significantly, except between DI and P1 patients (17.1% vs. 10.5%, P=0.344). The mean CEA values in SU, SE, DI, P1, and P2 patients were 5.80, 5.48, 13.36, 8.06, and 22.82, respectively. The CA19-9 values for these patients were 49.40, 38.97, 101.67, 73.77, and 98.57, respectively. The increase in CEA in P2 patients was statistically significant (P=0.002), and the increases in CA19-9 in DI and P2 patients were significant (P=0.025, 0.007, respectively). There was a fair correlation between the two markers in P2 patients (r=0.494, P<0.001). Conclusions: CA19-9 can be used to assess DI of gastric cancer into adjacent organs. Both markers are useful for predicting the presence of extensive peritoneal seeding.

• Journal of Life Science
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• v.28 no.1
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• pp.116-129
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• 2018

Living creatures possess long-conserved mechanisms to maintain homeostasis in response to various stresses. However, chronic and continuous exposure to stress can result in the excessive production of stress hormones, including catecholamines, which have harmful effects on health. Studies on the relationship between the sympathetic nervous system (SNS) and cancer have been conducted based on the traditional hypothesis that stress can promote cancer progression. Many preclinical and epidemiological studies have suggested that the regulation of ${\beta}$-adrenergic signaling, which mediates SNS activity, can suppress the progression of solid tumors. SNS activation has highly pleiotropic effects on tumor biology, as it stimulates oncogenes, survival pathways, the epithelial - mesenchymal transition, and invasion. Moreover, it inhibits DNA repair and programmed cell death and regulates the tumor microenvironment, including immune cells, endothelial cells, the extracellular matrix, mesenchymal cells, and adipocytes. Although targeted therapies on the molecular basis of tumor proliferation are currently receiving increased attention, they have clinical limitations, such as the compensatory activation of other signaling pathways, emergence of drug resistance, and various side effects, which raise the need for pleiotropic cancer regulation. This review summarizes the effects of the SNS on the development and progression of cancer and discusses the clinical perspectives of ${\beta}$-blockade as a novel therapeutic strategy for this disease.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5353-5361
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• 2012

Interleukin-18 (IL-18) is an immune-stimulatory cytokine with antitumor activity in preclinical models. It plays pivotal roles in linking inflammatory immune responses and tumor progression and is a useful candidate in gene therapy of lymphoma or lymphoid leukemia. A phase I study of recombinant human IL-18 (rhIL-18) in patients with advanced cancer concluded that rhIL-18 can be safely given in biologically active doses to patients with advanced cancer. Some viruses can induce the secretion of IL-18 for immune evasion. The individual cytokine activity might be potentiated or inhibited by combinations of cytokines. Here we focus on combinational effects of cytokines with IL-18 in cancer progression. IL-18 is an important non-invasive marker suspected of contributing to metastasis. Serum IL-18 may a useful biological marker as independent prognostic factor of survival. In this review we cover roles of IL-18 in immune evasion, metastasis and angiogenesis, applications for chemotherapy and prognostic or diagnostic significance.

• Reproductive and Developmental Biology
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• v.36 no.1
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• pp.39-47
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• 2012

Ovarian cancer is the most lethal gynecological malignancy, and specific biomarkers are important needed to improve diagnosis, prognosis, and to forecast and monitor treatment efficiency. There are a lot of pathological factors, including reactive oxygen species (ROS), involved in the process of cancer initiation and progression. The oxidative modification of proteins by ROS is implicated in the etiology or progression of disorders and diseases. In this study, a labeling experiment with the thiol-modifying reagent biotinylated iodoacetamide (BIAM) revealed that a variety of proteins were differentially oxidized between normal and tumor tissues of ovarian cancer patients. To identify cysteine oxidation-sensitive proteins in ovarian cancer patients, we performed comparative analysis by nano-UPLC-$MS^E$ shotgun proteomics. We found oxidation-sensitive 22 proteins from 41 peptides containing cysteine oxidation. Using Ingenuity program, these proteins identified were established with canonical network related to cytoskeletal network, cellular organization and maintenance, and metabolism. Among oxidation-sensitive proteins, the modification pattern of Collagen alpha-1(VI) chain (COL6A1) was firstly confirmed between normal and tumor tissues of patients by 2-DE western blotting. This result suggested that COL6A1 might have cysteine oxidative modification in tumor tissue of ovarian cancer patients.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.5
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• pp.487-498
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• 2016

Leptin, an adipokine predominantly produced from adipose tissue, is well known to induce tumor growth. However, underlying molecular mechanisms are not established yet. While p53 has long been well recognized as a potent tumor suppressor gene, accumulating evidence has also indicated its potential role in growth and survival of cancer cells depending on experimental environments. In the present study, we examined if p53 signaling is implicated in leptin-induced growth of cancer cells. Herein, we demonstrated that leptin treatment significantly increased p53 protein expression in both hepatic (HepG2) and breast (MCF-7) cancer cells without significant effect on mRNA expression. Enhanced p53 expression by leptin was mediated via modulation of ubiquitination, in particular ubiquitin specific protease 2 (USP2)-dependent manner. Furthermore, gene silencing of p53 by small interfering RNA (siRNA) suppressed leptin-induced growth of hepatic and breast cancer cells, indicating the role of p53 signaling in tumor growth by leptin. In addition, we also showed that knockdown of p53 restored suppression of caspase-3 activity by leptin through modulating Bax expression and prevented leptin-induced cell cycle progression, implying the involvement of p53 signaling in the regulation of both apoptosis and cell cycle progression in cancer cells treated with leptin. Taken together, the results in the present study demonstrated the potential role of p53 signaling in leptin-induced tumor growth.

• YAKHAK HOEJI
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• v.56 no.6
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• pp.358-363
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• 2012

Nemo-like kinase (NLK), an evolutionarily conserved serine/threonine protein kinase, plays an important role in wide variety of developmental events. NLK phosphorylates T-cell factor/lymphoid enhancer factor (TCF/LEF) transcriptional complex and suppresses wnt signaling pathway through inhibition of ${\beta}$-catenin/TCF complex interaction. However, the function of NLK in gastric carcinogenesis has not been investigated. In the present study, we have examined whether the NLK gene is involved in the development and/or progression of gastric cancers. NLK expression was analyzed by immunohistochemical staining in 153 advanced gastric cancer specimens. Immunhistochemical analysis showed increased expression of NLK in 91 (59.5%) out of 153 gastric cancer specimens. Statistically, there was no significant relationship between altered expression of NLK protein and clinicopathological parameters, including tumor differentiation, location, lymph node metastasis. We identified that mRNA and protein expression of NLK was significantly up-regulated in human gastric cancer tissues compare to corresponding normal gastric tissues. In addition, we found that human gastric cancer cell lines exhibited relatively high expression of NLK, as compared with normal gastric cells. The results of this study suggest that aberrant regulation of NLK may contribute to the development or progression of gastric cancers and serve as a potential biomarker for advanced gastric cancer patients.

• BMB Reports
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• v.52 no.6
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• pp.385-390
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• 2019

Leptin, an adipokine regulating energy metabolism, appears to be associated with breast cancer progression. Insulin-like growth factor-1 (IGF-1) mediates the pathogenesis of breast cancer. The regulation of IGF-1 expression by leptin in breast cancer cells is unclear. Here, we found that leptin upregulates IGF-1 expression at the transcriptional level in breast cancer cells. Activating protein-1 (AP-1)-binding element within the proximal region of IGF-1 was necessary for leptin-induced IGF-1 promoter activation. Forced expression of AP-1 components, c-FOS or c-JUN, enhanced leptin-induced IGF-1 expression, while knockdown of c-FOS or c-JUN abrogated leptin responsiveness. All three MAPKs (ERK1/2, JNK1/2, and p38 MAPK) mediated leptin-induced IGF-1 expression. These results suggest that leptin contributes to breast cancer progression through the transcriptional upregulation of leptin via the MAPK pathway.

• Journal of Ginseng Research
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• v.48 no.3
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• pp.266-275
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• 2024

Cancer stem cells (CSCs) are a rare subpopulation of cancer cells that exhibit stem cell-like characteristics, including self-renewal and differentiation in a multi-stage lineage state via symmetric or asymmetric division, causing tumor initiation, heterogeneity, progression, and recurrence and posing a major challenge to current anticancer therapy. Despite the importance of CSCs in carcinogenesis and cancer progression, currently available anticancer therapeutics have limitations for eradicating CSCs. Moreover, the efficacy and therapeutic windows of currently available anti-CSC agents are limited, suggesting the necessity to optimize and develop a novel anticancer agent targeting CSCs. Ginseng has been traditionally used for enhancing immunity and relieving fatigue. As ginseng's long history of use has demonstrated its safety, it has gained attention for its potential pharmacological properties, including anticancer effects. Several studies have identified the bioactive principles of ginseng, such as ginseng saponin (ginsenosides) and non-saponin compounds (e.g., polysaccharides, polyacetylenes, and phenolic compounds), and their pharmacological activities, including antioxidant, anticancer, antidiabetic, antifatigue, and neuroprotective effects. Notably, recent reports have shown the potential of ginseng-derived compounds as anti-CSC agents. This review investigates the biology of CSCs and efforts to utilize ginseng-derived components for cancer treatment targeting CSCs, highlighting their role in overcoming current therapeutic limitations.

• IMMUNE NETWORK
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• v.16 no.2
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• pp.85-98
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• 2016

The mitogen-activated protein kinases (MAPKs) are key regulators of cell growth and survival in physiological and pathological processes. Aberrant MAPK signaling plays a critical role in the development and progression of human cancer, as well as in determining responses to cancer treatment. The MAPK phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are a family of proteins that function as major negative regulators of MAPK activities in mammalian cells. Studies using mice deficient in specific MKPs including MKP1/DUSP1, PAC-1/DUSP2, MKP2/DUSP4, MKP5/DUSP10 and MKP7/DUSP16 demonstrated that these molecules are important not only for both innate and adaptive immune responses, but also for metabolic homeostasis. In addition, the consequences of the gain or loss of function of the MKPs in normal and malignant tissues have highlighted the importance of these phosphatases in the pathogenesis of cancers. The involvement of the MKPs in resistance to cancer therapy has also gained prominence, making the MKPs a potential target for anti-cancer therapy. This review will summarize the current knowledge of the MKPs in cancer development, progression and treatment outcomes.