• Journal of Korean Biological Nursing Science
• /
• 제3권1호
• /
• pp.11-28
• /
• 2001

This study was to identify the levels of perceived stress, immunity cells, physical health and depression, and their relationships among those variables in the elderly who institutionalized comparing home residents. The result of this study can be used as basic data when applying nursing interventions to increase quality of life in the elderly. The questionnaires to estimate stress, health status and depression were collected through direct interview from July to August in 1999 and immunity cells were measured by venous blood specimen collected from 9 to 10 A.M. during the same period. The collected data were analysed using SAS program. The results were as follows. The score of perceived stress of all subjects was 38.49 and perceived stress score of institutionalized elderly(42.62) was significantly higher than that in home resident elderly(34.52). All immune cells tested in this study such as total T cell, helper T cell, suppressor T cell, T4/T8 ration, total B cell, and NK cell, were all under the standard criteria of cells distributions. Most elderly who institutionalized and reside home replied that their health status was not good. However their physical health activity was mostly good even though institutionalized elderly had more disability than home residents. The highest rate was 67.3% as disability due to arthritis. The score of depression in all subjects was 8.2 that indicated having depressive symptom. There was no difference in the depression level between institutionalized elderly and home resided elderly. There was a significant correlationship between physical health and depression, however, the rest of varibles did not show any significant relationships. In summary, the immune cells in the elderly who replied perceiving low level stress, was under normal range. Their health status was perceived as 'not good' but physical health activity was perceived as 'good'. The relationships of stress, immunity, physical health and depression were partially significant but not had evidence as enough as theoretically the suggested relationship. We suggest that further studies using large sample size and more diverse variables should be performed.

• 대한핵의학회지
• /
• 제26권1호
• /
• pp.1-7
• /
• 1992

저자는 1991년 1월부터 동년 8월 사이에 부산대학교 병원 내과 외래에서 임상증상, 이학적 소견 및 각종 검사소견과 병리조직학적으로 진단된 단순 증식성 갑상선종 환자 20예, 갑상선선종 환자 9예 및 갑상선암환자 20예와 건강대조군 11례에서 말초혈 림프구의 PNP활성을 측정하고 $CD4^+$ 및 $CD8^+$ 세포를 동시에 검색하여 분석할 성적을 다음과 같이 요약한다. 1) 말초혈 림프구의 PNP 활성은 건강 대조군 및 단순 증식성 갑상선종 보다 갑상선선종 및 암환자에서 의의있게 증가하거나 증가하는 경향이 있었다. 2) 말초혈의 $CD8^+$ 세포 비율은 갑상선암환자에서 건강 대조군, 단순 증식성 갑상선종 및 갑상선선종환자 보다 각각 의의 있게 감소하거나 감소하는 경 향이 있었다. 3) 말초혈의 CD4/CD8비는 갑상선암환자에서 건강 대조군, 단순 증식성 갑상선종 및 갑상선선종환자보다 각각 의의 있게 증가하거나 증가하는 경향이 있었다. 이상의 결과에 의하면 갑상선암환자에서는 말초혈의 억제/세포상해 T 세포의 감소에 의한 세포성 면역능의 이상이 있고, 말초혈 림프구의 PNP활성의 측정은 갑상선종양환자의 면역 상태를 파악하는데 도움이 되는 검사라고 생각된다.

• BMB Reports
• /
• 제55권2호
• /
• pp.81-86
• /
• 2022

Macrophages are a major cellular component of innate immunity and are mainly known to have phagocytic activity. In the tumor microenvironment (TME), they can be differentiated into tumor-associated macrophages (TAMs). As the most abundant immune cells in the TME, TAMs promote tumor progression by enhancing angiogenesis, suppressing T cells and increasing immunosuppressive cytokine production. N-myc downstream-regulated gene 2 (NDRG2) is a tumor suppressor gene, whose expression is down-regulated in various cancers. However, the effect of NDRG2 on the differentiation of macrophages into TAMs in breast cancer remains elusive. In this study, we investigated the effect of NDRG2 expression in breast cancer cells on the differentiation of macrophages into TAMs. Compared to tumor cell-conditioned medium (TCCM) from 4T1-mock cells, TCCM from NDRG2-over-expressing 4T1 mouse breast cancer cells did not significantly change the morphology of RAW 264.7 cells. However, TCCM from 4T1-NDRG2 cells reduced the mRNA levels of TAM-related genes, including MR1, IL-10, ARG1 and iNOS, in RAW 264.7 cells. In addition, TCCM from 4T1-NDRG2 cells reduced the expression of TAM-related surface markers, such as CD206, in peritoneal macrophages (PEM). The mRNA expression of TAM-related genes, including IL-10, YM1, FIZZ1, MR1, ARG1 and iNOS, was also downregulated by TCCM from 4T1-NDRG2 cells. Remarkably, TCCM from 4T1-NDRG2 cells reduced the expression of PD-L1 and Fra-1 as well as the production of GM-CSF, IL-10 and ROS, leading to the attenuation of T cell-inhibitory activity of PEM. These data showed that compared with TCCM from 4T1-mock cells, TCCM from 4T1-NDRG2 cells suppressed the TAM differentiation and activation. Collectively, these results suggest that NDRG2 expression in breast cancer may reduce the differentiation of macrophages into TAMs in the TME.

• IMMUNE NETWORK
• /
• 제11권1호
• /
• pp.11-41
• /
• 2011

The discovery of microRNA (miRNA) is one of the major scientific breakthroughs in recent years and has revolutionized current cell biology and medical science. miRNAs are small (19~25nt) noncoding RNA molecules that post-transcriptionally regulate gene expression by targeting the 3' untranslated region (3'UTR) of specific messenger RNAs (mRNAs) for degradation of translation repression. Genetic ablation of the miRNA machinery, as well as loss or degradation of certain individual miRNAs, severely compromises immune development and response, and can lead to immune disorders. Several sophisticated regulatory mechanisms are used to maintain immune homeostasis. Regulatory T (Treg) cells are essential for maintaining peripheral tolerance, preventing autoimmune diseases and limiting chronic inflammatory diseases. Recent publications have provided compelling evidence that miRNAs are highly expressed in Treg cells, that the expression of Foxp3 is controlled by miRNAs and that a range of miRNAs are involved in the regulation of immunity. A large number of studies have reported links between alterations of miRNA homeostasis and pathological conditions such as cancer, cardiovascular disease and diabetes, as well as psychiatric and neurological diseases. Although it is still unclear how miRNA controls Treg cell development and function, recent studies certainly indicate that this topic will be the subject of further research. The specific circulating miRNA species may also be useful for the diagnosis, classification, prognosis of diseases and prediction of the therapeutic response. An explosive literature has focussed on the role of miRNA. In this review, I briefly summarize the current studies about the role of miRNAs in Treg cells and in the regulation of the innate and adaptive immune response. I also review the explosive current studies about clinical application of miRNA.

• Biomolecules & Therapeutics
• /
• 제26권1호
• /
• pp.4-9
• /
• 2018

Cancer metabolism as a field of research was founded almost 100 years ago by Otto Warburg, who described the propensity for cancers to convert glucose to lactate despite the presence of oxygen, which in yeast diminishes glycolytic metabolism known as the Pasteur effect. In the past 20 years, the resurgence of interest in cancer metabolism provided significant insights into processes involved in maintenance metabolism of non-proliferating cells and proliferative metabolism, which is regulated by proto-oncogenes and tumor suppressors in normal proliferating cells. In cancer cells, depending on the driving oncogenic event, metabolism is re-wired for nutrient import, redox homeostasis, protein quality control, and biosynthesis to support cell growth and division. In general, resting cells rely on oxidative metabolism, while proliferating cells rewire metabolism toward glycolysis, which favors many biosynthetic pathways for proliferation. Oncogenes such as MYC, BRAF, KRAS, and PI3K have been documented to rewire metabolism in favor of proliferation. These cell intrinsic mechanisms, however, are insufficient to drive tumorigenesis because immune surveillance continuously seeks to destroy neo-antigenic tumor cells. In this regard, evasion of cancer cells from immunity involves checkpoints that blunt cytotoxic T cells, which are also attenuated by the metabolic tumor microenvironment, which is rich in immuno-modulating metabolites such as lactate, 2-hydroxyglutarate, kynurenine, and the proton (low pH). As such, a full understanding of tumor metabolism requires an appreciation of the convergence of cancer cell intrinsic metabolism and that of the tumor microenvironment including stromal and immune cells.

• 대한한의학방제학회지
• /
• 제30권4호
• /
• pp.241-248
• /
• 2022

Objective : The purpose of this trial is to observe the preliminary effects of Salvia plebeia (SP) extract on quality of life in patients with solid cancer. Methods : This is a prospective, open-label, single-arm, and single-dose clinical trial. Twenty participants who have been diagnosed with solid cancer between the ages of 20 and 65 will be included. All participants will be administered SP granules for 12 weeks. Data will be collected at 4, 8, and 12 weeks after enrollment. The primary outcome is quality of life, using the Korean version of the Functional Assessment Cancer Therapy-General questionnaire. Secondary outcomes include tumor markers in blood tests for each cancer type, soluble programmed death-ligand 1, the percentage of natural killer cells among lymphocytes, ratio of T-helper and T-suppressor cells, ratio of total T, T-helper, T-suppressor, and B cells in lymphocytes, level of C-reactive protein, and tumor size via radiology examination. Safety will be assessed by clinical laboratory tests and monitoring of adverse events. Discussion : This study aims to observe the effects of an oral administration of SP preparations in patients with solid cancer on changes in quality of life and an improvement in immune function. It is expected to provide objective evidence of the effect and safety of SP for patients with solid cancer. Trial registration: KCT0007315 (Clinical Research Information Service)

• BMB Reports
• /
• 제55권8호
• /
• pp.380-388
• /
• 2022

The B cell translocation gene 1 (BTG1) and BTG2 play a key role in a wide range of cellular activities including proliferation, apoptosis, and cell growth via modulating a variety of central biological steps such as transcription, post-transcriptional, and translation. BTG1 and BTG2 have been identified by genomic profiling of B-cell leukemia and diverse lymphoma types where both genes are commonly mutated, implying that they serve as tumor suppressors. Furthermore, a low expression level of BTG1 or BTG2 in solid tumors is frequently associated with malignant progression and poor treatment outcomes. As physiological aspects, BTG1 and BTG2 have been discovered to play a critical function in regulating quiescence in hematopoietic lineage such as Hematopoietic stem cells (HSCs) and naive and memory T cells, highlighting their novel role in maintaining the quiescent state. Taken together, emerging evidence from the recent studies suggests that BTG1 and BTG2 play a central anti-proliferative role in various tissues and cells, indicating their potential as targets for innovative therapeutics.

• 대한미생물학회지
• /
• 제13권1호
• /
• pp.55-62
• /
• 1978

항암제(抗癌劑)로 잘 알려진 cyclophosphamide(CY)를 성숙(成熟)한 마우스에 체중(體重) kg당(當) 300mg을 복강내(腹腔內)에 투여(投與)하여 CY가 체중(體重), 비장중량(脾臟重量) 및 말초임파조직(末梢淋巴組織)에 미치는 영향(影響)을 실험(實驗)하였다. CY는 마우스의 체중(體重)을 약간(若干) 감소(減少)시켰으나 체중(體重)은 곧 회복(回復)되었다. CY가 비장중량(脾臟重量)에 미치는 영향(影響)은 현저(顯著)하였는데 초기(初期)엔 비장중량(脾臟重量)은 감소(減少)되었으나 곧 회복(回復)되고 그 후(後) 정상(正常)보다 더 증가(增加)되었는데 그 증가(增加)는 CY투여(投與) 20일(日)이 지나서야 정상(正常)으로 되돌아왔다. 비장(脾臟) 및 임파절(淋巴節)의 조직학적(組織學的) 형태(形態)에 미치는 CY의 영향(影響)은 다양(多樣)하였다. 즉(卽), 흉선의존세포(胸線依存細胞)가 위치(位置)하는 비장(脾臟)의 periarterial lymphatic sheath와 임파절(淋巴節)의 paracortex는 골수유래세포(骨髓由來細胞)가 위치(位置)하는 follicles보다 1일(日) 내지(乃至) 2일(日) 늦게 소실(消失)되었으며 비장(脾臟)의 비대(肥大)가 최고(最高)에 달(達죠)하였을때 비장(脾臟)이나 임파절(淋巴節)의 구조(構造)는 동일(同一)한 임파양세포(淋巴樣細胞)로 구성(構成)된 interstitial tissue로 대치(代置)되어 있었다. 비장(脾臟)의 중량(重量)이 정상화(正常化)되어감에 따라 비장(脾臟)이나 임파절(淋巴節)의 구조(構造)가 정상화(正常化) 되어갔다. 이와 같은 본(本) 실험(實驗)의 소견(所見)은 CY는 골수유래세포(骨髓由來細胞) 뿐만 아니라 흉선의존세포(胸線依存細胞)에도 영향(影響)을 미친다고 사료(思料)된다. 저자(著者)들은 전보(前報)에서 CY에 의(依)한 지연성과민반응(遲延性過敏反應)의 항진(亢進)은 suppressor T cell의 제거(除去)에 기인(基因)한 것이라고 시사(示唆)하였는데 본(本) 실험결과(實驗結果)는 이를 뒷받침해준다고 사료(思料)되었다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제24권3호
• /
• pp.203-212
• /
• 2020

Promyelocytic leukemia (PML) gene, through alternative splicing of its C-terminal region, generates several PML isoforms that interact with specific partners and perform distinct functions. The PML protein is a tumor suppressor that plays an important role by interacting with various proteins. Herein, we investigated the effect of the PML isoforms on oncostatin M (OSM)-induced signal transducer and activator of transcription-3 (STAT-3) transcriptional activity. PML influenced OSM-induced STAT-3 activity in a cell type-specific manner, which was dependent on the p53 status of the cells but regardless of PML isoform. Interestingly, overexpression of PML exerted opposite effects on OSM-induced STAT-3 activity in p53 wild-type and mutant cells. Specifically, overexpression of PML in the cell lines bearing wild-type p53 (NIH3T3 and U87-MG cells) decreased OSM-induced STAT-3 transcriptional activity, whereas overexpression of PML increased OSM-induced STAT-3 transcriptional activity in mutant p53-bearing cell lines (HEK293T and U251-MG cells). When wild-type p53 cells were co-transfected with PML-IV and R273H-p53 mutant, OSM-mediated STAT-3 transcriptional activity was significantly enhanced, compared to that of cells which were transfected with PML-IV alone; however, when cells bearing mutant p53 were co-transfected with PML-IV and wild-type p53, OSM-induced STAT-3 transcriptional activity was significantly decreased, compared to that of transfected cells with PML-IV alone. In conclusion, PML acts together with wild-type or mutant p53 and influences OSM-mediated STAT-3 activity in a negative or positive manner, resulting in the aberrant activation of STAT-3 in cancer cells bearing mutant p53 probably might occur through the interaction of mutant p53 with PML.

• Molecules and Cells
• /
• 제43권7호
• /
• pp.619-631
• /
• 2020

In this study, we describe a novel function of TNNC1 (Troponin C1, Slow Skeletal and Cardiac Type), a component of actin-bound troponin, as a tumor suppressor of lung adenocarcinoma (LUAD). First, the expression of TNNC1 was strongly down-regulated in cancer tissues compared to matched normal lung tissues, and down-regulation of TNNC1 was shown to be strongly correlated with increased mortality among LUAD patients. Interestingly, TNNC1 expression was enhanced by suppression of KRAS, and ectopic expression of TNNC1 in turn inhibited KRAS^G12D-mediated anchorage independent growth of NIH3T3 cells. Consistently, activation of KRAS pathway in LUAD patients was shown to be strongly correlated with down-regulation of TNNC1. In addition, ectopic expression of TNNC1 inhibited colony formation of multiple LUAD cell lines and induced DNA damage, cell cycle arrest and ultimately apoptosis. We further examined potential correlations between expression levels of TNNC1 and various clinical parameters and found that low-level expression is significantly associated with invasiveness of the tumor. Indeed, RNA interference-mediated down-regulation of TNNC1 led to significant enhancement of invasiveness in vitro. Collectively, our data indicate that TNNC1 has a novel function as a tumor suppressor and is targeted for down-regulation by KRAS pathway during the carcinogenesis of LUAD.