Ji-Hye Jung, Ji-Young Kim, Suji Jeong, Ji Yoon Lee, Seon-Sook Han, Seok-Ho Hong
{"title":"Glyoxalase 1 (GLO1) Deficiency Is Associated with Myeloid Skewing and Altered Inflammatory Responses.","authors":"Ji-Hye Jung, Ji-Young Kim, Suji Jeong, Ji Yoon Lee, Seon-Sook Han, Seok-Ho Hong","doi":"10.12717/DR.2026.30.3.145","DOIUrl":"10.12717/DR.2026.30.3.145","url":null,"abstract":"<p><p>Glyoxalase 1 (GLO1) is involved in cellular adaptation to metabolic and oxidative stress, however, its role in regulating immune homeostasis remains poorly understood. Here, we used <i>Glo1</i> knockout (Glo1-KO) mice to investigate the effects of GLO1 deficiency on bone marrow (BM) hematopoietic composition and the pulmonary inflammation environment. Flow cytometric analysis revealed alterations in BM myeloid-derived suppressor cell population, in Glo1-KO mice. In the lung GLO1 deficiency was accompanied by increased expression of inflammation and tissue-remodeling-associated genes, indicating an altered pulmonary inflammation milieu. Together, these findings demonstrate that GLO1 deficiency is associated with coordinated changes in hematopoietic immune environments and suggest that GLO1 may influence immune regulation across hematopoietic and peripheral tissue compartments.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 3","pages":"145-153"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Reconstructing the Human Endometrium <i>In Vitro</i>: Current Three-Dimensional (3D) Models and Future Perspectives.","authors":"Se-Hee Han, Yong-Pil Cheon","doi":"10.12717/DR.2026.30.3.121","DOIUrl":"10.12717/DR.2026.30.3.121","url":null,"abstract":"<p><p>There are differences between artificial 3D systems and ex vivo model systems, but they are same in trying to mimic the similarity to <i>in vivo</i> tissue or organs, here we put them in a 3D model. This review summarizes current 3D endometrial models, including extracellular matrix (ECM) and hydrogel-based systems, endometrial organoids and assembloids, and advanced engineered platforms such as microfluidic organ-on-a-chip systems and 3D bioprinting, as well as advanced <i>ex vivo</i> organotypic, native-preserved 3D systems. These models have enabled the investigation of endometrial functions, including hormone-dependent epithelial differentiation, stromal decidualization, epithelial-stromal crosstalk, and trophoblast invasion, as well as embryo-endometrium interactions. Despite these advances, individual models reproduce only selected biochemical, cellular, spatial, or dynamic features of the native endometrium, and challenges remain in achieving physiological relevance together with reproducibility, standardization, and experimental accessibility. This review further argues that future 3D endometrial models should balance physiological relevance with reproducibility, standardization, and experimental accessibility, rather than simply increasing model complexity. Such models may provide improved platforms for studying uterine endometrial physiology, implantation, and reproductive disorders.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 3","pages":"121-134"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Catenin Alpha-Like 1 (CTNNAL1) Modulates Cancer Stem Cell-Associated Properties and Epithelial-Mesenchymal Transition (EMT)-Associated Phenotypes in MDA-MB-231 Breast Cancer Cells.","authors":"Min Su Kim, Jin Young Jang, Rae-Kwon Kim","doi":"10.12717/DR.2026.30.3.135","DOIUrl":"10.12717/DR.2026.30.3.135","url":null,"abstract":"<p><p>Catenin alpha-like 1 (CTNNAL1) is an adhesion-related protein implicated in cellular plasticity; however, its involvement in cancer stem cell (CSC)-associated properties and epithelial-mesenchymal transition (EMT)-associated phenotypes in breast cancer remains unclear. In this study, we investigated the relationship of CTNNAL1 with CSC-associated properties and EMT-associated phenotypes in MDA-MB-231 breast cancer cells. CTNNAL1 expression increased under sphere-forming conditions together with CSC-associated markers, including CD44, aldehyde dehydrogenase 1 (ALDH1A1), and ALDH1A3. Silencing of CTNNAL1 reduced the expression of these markers and stemness-associated transcription factors, including Sox2, Oct4, and Nanog. CTNNAL1 knockdown also decreased sphere size and sphere-forming efficiency. Furthermore, CTNNAL1 depletion increased E-cadherin expression and decreased N-cadherin, vimentin, and EMT-associated transcription factors, including Snail, Slug, Twist, and ZEB1. CTNNAL1 knockdown also reduced cell migration and invasion. Collectively, these findings suggest that CTNNAL1 is associated with CSC-like properties and EMT-associated phenotypes in MDA-MB-231 breast cancer cells.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 3","pages":"135-144"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Facial Cartilage Development in Jawed Fish.","authors":"Sil Jin, Yucheol Choe, Chong Pyo Choe","doi":"10.12717/DR.2026.30.3.113","DOIUrl":"10.12717/DR.2026.30.3.113","url":null,"abstract":"<p><p>In jawed fish, the jaw and branchial basket are essential organs for respiration and feeding. During embryogenesis, facial cartilages that form the framework of the jaw and branchial basket are developed from the cranial neural crest-derived ectomesenchyme of the pharyngeal arches. Developmental genetic studies in zebrafish and skates reveal that, in the jaw, the developmental processes for facial cartilage formation are largely conserved. While those for the development of cartilaginous elements of the branchial basket are less understood, recent studies in zebrafish suggest a unique developmental genetic basis for dorsal cartilaginous elements of the branchial basket. In this mini-review, we sketch the developmental genetic processes for facial cartilage formation in the jawed fish, together with recent discoveries on the dorsal cartilage development in the zebrafish branchial basket.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 3","pages":"113-120"},"PeriodicalIF":0.0,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13678310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Baculoviral Inhibitor of Apoptosis Repeat Containing 5 (BIRC5) Regulates Cancer Stem Cell Properties and Epithelial-Mesenchymal Transition in Human Breast Cancer Cells.","authors":"Jin Young Jang, Rae-Kwon Kim","doi":"10.12717/DR.2026.30.2.95","DOIUrl":"10.12717/DR.2026.30.2.95","url":null,"abstract":"<p><p>Baculoviral inhibitor of apoptosis repeat containing 5 (BIRC5) (survivin) is known to play an important role in cell survival and tumor progression; however, its involvement in cancer stem cell (CSC) properties and epithelial-mesenchymal transition (EMT) in breast cancer remain unclear. In this study, we investigated the role of BIRC5 in regulating CSC-like characteristics and EMT in human breast cancer cells. Analysis of public datasets revealed that BIRC5 expression is significantly elevated in breast cancer tissues and is associated with poor patient prognosis. Treatment with CSC-inducing conditioned medium (CSC-CM) increased the expression of CSC markers, including CD44, ALDH1A1, and ALDH1A3. Silencing of BIRC5 using siRNA reduced the expression of CSC-associated markers as well as pluripotency-related transcription factors (Sox2, Oct4, and Nanog). In addition, BIRC5 knockdown significantly decreased sphere-forming ability, indicating reduced self-renewal capacity. Furthermore, suppression of BIRC5 altered EMT-related protein expression, as evidenced by increased E-cadherin and decreased N-cadherin, Vimentin, and EMT-associated transcription factors (Snail, Slug, Twist, and Zeb1). In addition, BIRC5 knockdown also significantly reduced cell migration and invasion. These results suggest that BIRC5 is involved in the regulation of CSC properties and EMT in breast cancer cells and may contribute to tumor progression.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 2","pages":"95-104"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148439029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lin28 Represses Hub Cell microRNAs to Maintain <i>Drosophila</i> Testis Niche Function.","authors":"Perinthottathil Sreejith, Changsoo Kim","doi":"10.12717/DR.2026.30.2.105","DOIUrl":"10.12717/DR.2026.30.2.105","url":null,"abstract":"<p><p>In the <i>Drosophila</i> testis, hub cells form a specialized niche that sustains adjacent stem cells. The RNA-binding protein Lin28 is expressed in hub cells and is essential for their maintenance and niche function; however, the underlying mechanisms remain poorly understood. Lin28 is well-characterized as a suppressor of <i>let-7</i> biogenesis, raising the possibility that Lin28 regulates <i>let-7</i> and additional microRNAs to preserve hub cell identity. We performed genome-wide microRNA expression profiling and identified a set of microRNAs upregulated in <i>lin28</i> mutant testes, including <i>let-7</i>, demonstrating that Lin28 represses <i>let-7</i> in hub cells to protect <i>let-7</i>-targeted hub cell factors. Here, we report genetic analysis of <i>miR-304</i>, a microRNA identified from the profiling. <i>miR-304</i> contains a seed site complementary to the 3' UTR of the IGF-II mRNA-binding protein (IMP), a critical hub-specific factor. We find that <i>miR-304</i> mutant testes exhibit elevated levels of IMP specifically in hub cells, suggesting that <i>miR-304</i> targets <i>imp</i> mRNAs and reduces <i>imp</i> expression in hub cells. Thus, in wild-type hub cells, Lin28 represses <i>miR-304</i> to maintain IMP expression. We propose that Lin28 preserves niche function by restraining multiple microRNAs, thereby protecting essential hub cell factors from microRNA-mediated silencing.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 2","pages":"105-112"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148439100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hyo Gyeong Yun, Eun Bin Song, Dong Hoon Kwak, Ki Kwan Kim, Min Young Kim, Young-Kug Choo
{"title":"Inflammation Disrupts Ganglioside Expression during Early Embryonic Development in Institute of Cancer Research (ICR) Mice: Protective Effects of Melatonin.","authors":"Hyo Gyeong Yun, Eun Bin Song, Dong Hoon Kwak, Ki Kwan Kim, Min Young Kim, Young-Kug Choo","doi":"10.12717/DR.2026.30.2.79","DOIUrl":"10.12717/DR.2026.30.2.79","url":null,"abstract":"<p><p>Inflammation adversely affects reproductive function and early embryonic development; however, whether inflammatory conditions are associated with alterations in ganglioside expression during early embryogenesis remains unclear. The present study aimed to investigate whether lipopolysaccharide (LPS)-induced chronic inflammation is associated with alterations in ovarian function and early embryonic developmental competence in Institute of Cancer Research (ICR) mice, and whether subsequent melatonin intervention is accompanied by a partial recovery trend. Embryonic developmental competence was evaluated by superovulation and <i>in vitro</i> fertilization (IVF), and GM3 levels along with <i>ST3GAL5</i> expression in ovarian tissues and blastocyst-stage embryos were assessed using biochemical analysis and immunofluorescence staining. LPS-induced inflammation was associated with reduced oocyte recovery, decreased blastocyst formation rates, and lower GM3 band intensities and <i>ST3GAL5</i> fluorescence signals in ovarian tissues and embryos. Melatonin treatment partially improved reproductive outcomes and was accompanied by a partial recovery trend in GM3 levels and <i>ST3GAL5</i> expression. These findings suggest that melatonin may partially alleviate LPS-induced reproductive impairment, and that recovery of <i>ST3GAL5</i>/GM3-related expression may be associated with this partial mitigating trend. However, the present study does not establish a direct causal relationship between these molecular changes and improved embryonic development.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 2","pages":"79-93"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148439062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Localization of Luteinizing Hormone (LH) Subunits Like Substances in the Mouse Placenta.","authors":"Eun Hye Ko, Sung-Ho Lee","doi":"10.12717/DR.2026.30.2.71","DOIUrl":"10.12717/DR.2026.30.2.71","url":null,"abstract":"<p><p>Luteinizing hormone (LH) is a vital reproductive hormone produced by the anterior pituitary gland, essential for both fertility and sexual development. Interestingly, there is evidence indicates that rodent placenta is extrapituitary site of LH synthesis. On this basis, we performed immunohistochemistry (IHC) using specific antisera for LH subunits to investigate the tissue distribution of the LH subunits like molecules in mice placentae. Pregnant mice on gestation day 17 were sacrificed and the placentae were obtained Glycogen rich trophoblast cells (GlyT) in the junctional zone (JZ) were positive for CGα immunohistochemical staining, and the LH-β positive staining was found in all cell layers in both JZ and labyrinth zone (LZ). Immunoreactive LH-receptor (LH-R) staining was observed on the membrane of GlyT in JZ and partial syncytiotrophoblast cells layer in LZ. The present study demonstrated that immunoreactive LH subunits like substances were localized differentially in the microstructures of mice placentae. This finding that the substances exhibiting immune responses to these and their receptors exist in the same type of cells and/or adjacent cells, suggesting the possibility of local regulation through these substances. Further studies will be helpful for understanding the biochemical nature and the role(s) of local LH-like substances in sophisticated placental physiology.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 2","pages":"71-77"},"PeriodicalIF":0.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148439158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Genetic Anatomy and Ontogenetic Roles of Early Growth Response 1 (Egr1) in Human and Mouse.","authors":"In-Ha Na, Yong-Pil Cheon","doi":"10.12717/DR.2026.30.1.1","DOIUrl":"10.12717/DR.2026.30.1.1","url":null,"abstract":"<p><p>The early growth response 1 (<i>Egr1</i>) gene is a well-known immediate-early gene in the <i>Egr</i> family. It encodes cysteine-2-histidine-2 (C2H2)-type zinc-finger DNA binding domain. EGR1 is involved in various developmental processes, including cell proliferation, differentiation, inflammation, neuroplasticity, angiogenesis, and endocrine. <i>Egr1</i> deficiency causes infertility due to impaired ovulation associated with the non-expression of LHβ. It has also been suggested that EGR1 may be essential for endometrial differentiation. Interestingly, EGR1 suppresses or activates the expression of downstream genes, depending on the cellular environment and stimuli. This is suspected to be influenced by the level of EGR1, its structure, and its interactions with other transcription regulators. <i>Egr1</i> gene is constructed with 2 exons and 1 intron without alternative spliced transcripts in both human and mouse. <i>Egr1</i> expression is under the control of itself and other <i>cis</i>- and <i>trans</i>-factors. <i>Egr1</i> has one promoter and a few enhancers with differences between human and mouse. The promoter contains binding sites for various transcription factors, including EGR1, activator protein 1 (AP1), EGR1 binding site (EBS), and specificity protein 1 (SP1). TATA and CAT boxes are present in the mouse Egr1 gene, but the TATA box is found only in humans. EGR1 is also suggested as a target for treatment for some diseases, like cancer, but it requires much more basic knowledge. Understanding EGR1's cell type-specific functions at the various levels will be helpful in understanding the normal development and in finding therapeutic targets in reproduction, cancer, and immune-related diseases. In this review, we briefly summarize the genetic anatomy with the molecular and developmental roles of EGR1.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 1","pages":"1-23"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13086562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Estrogen Regulates Microtubule-Associated Protein 1 Light Chain 3 in Mouse Uterine Endometrial Epithelium.","authors":"Sohyeon Moon, Soohyung Lee, Youngsok Choi","doi":"10.12717/DR.2026.30.1.25","DOIUrl":"10.12717/DR.2026.30.1.25","url":null,"abstract":"<p><p>Microtubule-associated protein 1 light chain 3 (LC3) belongs to the ATG8 family and plays a crucial role in regulating the induction of autophagy. Autophagy proceeds via the conversion of LC3B-I to LC3B-II, which is degraded during the fusion of autophagosomes and lysosomes. Uterine autophagy is regulated by ovarian steroid hormones. However, the mechanism governing late-stage autophagic maturation (autophagosome-lysosome fusion) in the uterus remains unclear. We have previously reported that the activity and expression of serine/threonine protein kinase 4 (STK4) are regulated by estrogen (E<sub>2</sub>) in the uterine epithelium. In the present study, we investigated the regulatory role of STK4 in autolysosome formation via LC3. We found that estrogen treatment reduced LC3B-II within three hours, but not LC3B-I, suggesting regulation at the late-stage autophagic maturation step, without evidence of suppressed autophagosome formation. Treatment with the estrogen receptor antagonist ICI 182,780 clearly reversed the reduction in LC3B-II caused by E<sub>2</sub>. Furthermore, we discovered that STK4 knockdown decreased the phosphorylation of threonine at the 50th position of the LC3B protein. Finally, we observed that LC3B phosphorylation plays a role in autolysosome formation rather than in autophagosome formation. These findings imply that late-stage autophagic maturation in the uterine epithelium is regulated by LC3B phosphorylation via estrogen and STK4. This will improve our understanding of uterine dynamics via the regulation of autophagy during the estrous cycle.</p>","PeriodicalId":72791,"journal":{"name":"Development & reproduction","volume":"30 1","pages":"25-38"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13077504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147693996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}