Uncovering tumor markers of colorectal cancer is important for the early detection and prognosis of the patients. Spermine oxidase (SMOX) is upregulated in various cancers. The present study aims to explore the biologic function and expression patterns of SMOX in colorectal cancer (CRC), the third most common type of cancer worldwide. We used quantitative real-time PCR, Western blot, and in vitro functional studies in four CRC cell lines knocked down by SMOX siRNA and immunohistochemistry in 350 cases of CRC tissues. The results showed that SMOX was overexpressed in CRC cell lines and clinical samples. SMOX overexpression in tumor tissues was an independent prognostic factor, worsening overall survival (p = 0.001). The knock-down of SMOX inhibited CRC cell proliferation, invasion, and soft agar colony formation, uncovering its carcinogenic functions. This study indicated that SMOX overexpression could be an important oncogene in CRC and might serve as a valuable prognostic marker and potential therapeutic target for CRC.

Cancer is a major disease and the leading cause of death worldwide, with colorectal cancer (CRC) being the third-most common cancer in Korea. The survival rate associated with CRC reduces as the disease stage increases. Therefore, its early detection and treatment can greatly increase patient survival rates. In this study, we identified the tetraspanin 5 (TSPAN5) gene as an important biomarker for predicting the prognosis of patients with CRC. A TMA slide was used for statistical analysis. pN and clinical stage were found to be significant factors according to chi-square analysis, whereas pT, pN, metastasis, clinical stage, and TSPAN5 expression were significant according to Cox regression analysis. In order to prove the usefulness of TSPAN5, which is overexpressed in patients with metastatic CRC, as a biomarker, proliferation, migration, invasion, and tumorigenicity were examined using cell lines inhibited using small interfering RNA. The evaluations confirmed that TSPAN5 suppression, in turn, suppressed proliferation, migration, invasion, and tumorigenesis, which are characteristic of cancer cells. Therefore, the evaluation of TSPAN5 expression may help observe the prognosis of CRC and determine an appropriate treatment method for patients with CRC.

Background: Chronic obstructive pulmonary disease (COPD) develops through heterogeneous lung-function trajectories, but the longitudinal role of preserved ratio impaired spirometry (PRISm) in progression toward COPD remains unclear. Objective: We aimed to characterize long-term spirometric trajectories and transitions from normal spirometry to PRISm or COPD in a population-based cohort. Patients and Methods: We analyzed data from the Ansan–Ansung cohort of the Korean Genome and Epidemiology Study. Among medication-free participants with normal baseline spirometry who had classifiable spirometry across seven examinations over approximately 12 years, longitudinal trajectories of forced expiratory volume in 1 second (FEV₁, % predicted) and the FEV₁/FVC ratio were evaluated. Participants were classified into normal maintenance, PRISm, or COPD trajectory groups using a clinically interpretable, rule-based approach. Because post-bronchodilator measurements were not available across all examinations, COPD was operationally defined using pre-bronchodilator spirometry as FEV₁/FVC < 0.70. Results: Lung-function decline followed heterogeneous trajectories rather than a single linear pathway. Among 1,753 participants, 1,658 (94.6%) remained normal, 21 (1.2%) developed PRISm, and 74 (4.2%) progressed to COPD. Most individuals who developed COPD did so without a preceding sustained PRISm phase. In descriptive baseline comparisons, the COPD trajectory showed greater smoking exposure, higher blood pressure, and more pronounced central adiposity, whereas PRISm was more closely associated with wheeze-related respiratory symptoms and lower baseline lung function. In multivariable logistic regression, older age and current smoking were the strongest independent predictors of progression to COPD. Conclusion: Progression toward COPD in the general population is heterogeneous, and PRISm is not an obligatory precursor to COPD. Longitudinal spirometric assessment may provide clinically relevant insights beyond single time-point classification in the general population. Plain Language Summary: Why was the study done? COPD does not develop in the same way in everyone. Preserved ratio impaired spirometry (PRISm) has been proposed as an early stage of COPD, but its long-term role remains uncertain. This study examined how lung function changes over time and whether PRISm always leads to COPD. What did the researchers do? We studied Korean adults from the general population who had normal lung function at baseline. Lung function was measured seven times over about 12 years using spirometry. We tracked each person’s lung-function pattern over time and grouped participants according to their long-term trajectories. What did the researchers find? Lung-function change was heterogeneous. Most participants remained normal, some developed PRISm, and a smaller group developed COPD. Many individuals who developed COPD did so without a sustained PRISm phase. The COPD trajectory was more strongly associated with older age and smoking, and descriptively showed less favorable baseline clinical profiles, whereas PRISm was more closely associated with wheeze-related symptoms and lower baseline lung function. What do these results mean? PRISm is not always a necessary step before COPD. Repeated spirometry over time may provide more useful information than a single test for identifying people at risk of COPD and for understanding different pathways of disease development.

Chronic obstructive pulmonary disease (COPD) is influenced by environmental exposure and genetic susceptibility. Although large-scale genetic studies have identified loci associated with COPD and lung function, most evidence has come from populations of European ancestry, and data from Asian populations remain limited. This scoping review aimed to summarize KoGES-based studies on genetic and epigenetic associations with COPD and COPD-related lung function phenotypes. PubMed, Scopus, Web of Science, KoreaMed, RISS, KISS, and DBpia were searched from inception to April 27, 2026. Original studies using KoGES data to investigate genetic or epigenetic associations with COPD, airflow limitation, lung function traits, or longitudinal lung function decline were included. The review followed the Arksey and O’Malley framework and PRISMA-ScR guidance. Of 20 unique records identified for final assessment, one conference abstract/preliminary report corresponding to a subsequently published full-length article was removed before screening. The remaining 19 records were screened, and 12 studies met the eligibility criteria. Most KoGES-based studies focused on spirometric traits, including FEV1, FEV1/FVC, and longitudinal lung function decline, rather than clinically defined COPD. Major approaches included genome-wide association studies (GWAS), exome array analysis, gene–environment interaction, polygenic/genetic risk score (PRS/GRS) analysis, epigenome-wide association studies (EWAS), and heritability analysis. Recurrent signals involved FAM13A and the 6p21/AGER region. Recent studies increasingly addressed longitudinal phenotypes, including rapid FEV1 decline and annual lung function decline. KoGES-based studies provide population-specific evidence on genetic and epigenetic associations with COPD-related lung function phenotypes in Koreans. However, evidence for clinically defined COPD, externally validated risk prediction, and integrative multi-omics remains limited. Future studies should distinguish spirometric traits, longitudinal decline, and clinically defined COPD while validating KoGES findings in larger Asian and multi-ethnic populations. COPD develops through a combination of smoking, environmental exposure, and genetic susceptibility. Most large genetic studies on COPD have been conducted in European populations, so less is known about genetic factors in Koreans. We reviewed studies that used data from the Korean Genome and Epidemiology Study (KoGES) to understand what is already known and what research gaps remain. We searched major Korean and international databases for studies that used KoGES data to investigate genetic or epigenetic factors related to COPD or lung function. We then grouped the studies by research type, such as genome-wide association studies, exome-based studies, polygenic risk score studies, interaction studies, and methylation studies. Most KoGES-based studies focused on lung function measurements such as FEV1 and FEV1/FVC rather than clinically diagnosed COPD alone. Repeated evidence was found for several loci, especially FAM13A and the 6p21 region. More recent studies have moved from cross-sectional analyses toward longitudinal outcomes, such as rapid lung function decline and annual change in lung function. Some studies have also begun to evaluate polygenic risk and its interaction with modifiable lifestyle factors. KoGES has helped improve understanding of genetic influences on lung function in Koreans, but important gaps remain. There are still relatively few studies on clinically defined COPD, externally validated genetic risk prediction, and multi-omics integration. More longitudinal and population-specific studies are needed to support future research on early identification, external validation, and prevention-related research questions.