https://ir.ymlib.yonsei.ac.kr/handle/22282913/168741 2026-06-13T04:15:06Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/210210 Title: Impact of gut microbiota on host stem cells across the gastrointestinal tract Authors: Jeong, Haengdueng; Lee, Yura; Nam, Ki Taek; 이유라 Abstract: The gut microbiota plays a pivotal role in maintaining gastrointestinal (GI) homeostasis by influencing epithelial integrity, immunity, and metabolism. Recent studies have uncovered that gut microbiota can directly or indirectly modulate the behavior and function of adult stem cells across the GI tract, which are essential for tissue regeneration and disease prevention. Moreover, key microbial metabolites including short-chain fatty acids (SCFAs), tryptophan-derived indoles, succinate, secondary bile acids, and retinoic acid exert diverse effects on stem cell quiescence, proliferation, and differentiation. This review provides current knowledge on the interaction between gut microbiota and host stem cells in the stomach, intestine, and colon. 2026-12-01T00:00:00Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/211412 Title: ATP release mediated by TRPM3 enhances invasion in glioblastoma Authors: Bae, Kkot Garam; Song, Chae Won; Yoo, Jae Hong; Lee, Myunghoon; Koo, Noah; Lee, Gangsan; Park, Yongmin Mason; Yoo, Jihwan; Hwang, In-Young; Woo, Dong Ho; Lee, C. Justin; Han, Kyung-Seok Abstract: Glioblastoma (GBM) is the most aggressive and lethal form of primary brain tumor, characterized by uncontrolled proliferation and invasion into surrounding brain tissue. Mechanical stimulation (MS) in the tumor microenvironment (TME) has been correlated to tumor progression, partly via ATP release. However, the underlying molecular mechanisms remain poorly understood. In this study, we found that transient receptor potential melastatin 3 (TRPM3) channel mediates MS-induced ATP release from GBM cells. Genetic knockdown of TRPM3 significantly attenuated ATP release and suppressed GBM cell invasion, indicating its functional relevance in tumor dissemination. Furthermore, TRPM3 regulated ATP release in a Ca2+-independent manner, suggesting a noncanonical mechanism of mechanosensitive signaling. Consequently, targeting TRPM3 may offer a novel target to reduce the invasion of GBM within the TME. 2026-12-01T00:00:00Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/211708 Title: The effects of nanopillar and nanopit arrays on the morphology and osteogenic differentiation of adipose-derived stem cells Authors: Kang, Jihun; Yun, Young-Shik; Kang, Eun-Hye; Lee, Jihye; Jeon, Deok-Jin; Ji, Seungmuk; Kim, Yong-Oock; Yun, In-Sik; Yeo, Jong-Souk Abstract: Nanotopographic control of cell behavior offers great potential in designing biomimetic scaffolds for cell therapy. However, the behavior of cells on different nanotopographies is not fully understood. In this study, we investigated the effect of nanostructures on human adipose-derived stem cells (ASCs) by directly comparing nanopillar and nanopit arrays. Morphological changes, cell viability and early osteogenic differentiation of ASCs have been analyzed on the nanostructures. Nanopit arrays were found to increase cell areas and promote early osteogenic differentiation more than nanopillar arrays. Analysis of focal adhesion (FA) formation indicated a larger increase in total area as well as the number of FAs during cell spreading on nanopit arrays. The maturation of FA is related to cellular traction forces, which are known to stimulate osteogenic induction through the RhoA-ROCK pathway. We conclude that ASCs can spread more on the nanopit array than on the nanopillar array due to the presence of continuous adhesive paths on the nanopit array, which is associated with increased expression of RUNX2 as an early osteogenic marker. Our results suggest that a connected path in nanopit arrays plays a critical role in controlling stem cell behavior compared to nanopillar arrays. A comparative understanding of nanostructures can provide a guideline for designing an artificial substrate for osteogenesis and tissue engineering. © The Author(s) 2026. 2026-12-01T00:00:00Z https://ir.ymlib.yonsei.ac.kr/handle/22282913/211870 Title: Application and mechanistic research of novel therapeutic strategies in cisplatin-resistant small cell lung cancer Authors: Chen, Zhe; Qiang, Min; Dong, Junxue; Gong, Kejian; Zhang, Xinjun; Huo, Peng; Zhu, Jingjun; Shao, Yifeng; Ma, Jianzun; Zhang, Bowei; Liu, Wei; Tang, Mingbo Abstract: IntroductionSmall cell lung cancer (SCLC) initially responds well to cisplatin-based chemotherapy, but rapid development of drug resistance limits long-term efficacy and subsequent treatment options. Understanding the multifactorial mechanisms of cisplatin resistance is essential for improving patient outcomes. This review synthesizes recent preclinical and clinical advances, focusing on seven key resistance mechanisms and emerging therapeutic strategies, including immunotherapy, targeted therapy, and novel chemotherapeutic agents.DiscussionCisplatin resistance in SCLC arises through multiple mechanisms. First, reduction of drug deposition due to altered uptake or enhanced efflux decreases intracellular cisplatin levels. Second, dysregulation of apoptotic pathways, including overexpression of anti-apoptotic proteins such as Bcl-2, allows tumor cells to evade chemotherapy-induced cell death. Third, enhanced DNA damage repair restores cisplatin-induced lesions, limiting cytotoxicity. Fourth, the tumor microenvironment can induce resistance through stromal and immune interactions. Fifth, metabolic adaptations enable tumor cells to survive under chemotherapeutic stress. Sixth, SCLC subtype transitions alter cellular phenotype and chemosensitivity. Seventh, epigenetic changes drive transcriptional programs that confer resistance.Targeted therapies, such as multidrug resistance (MDR) inhibitors and Bcl-2 family inhibitors, can restore tumor sensitivity but are limited by toxicity and tumor-specific efficacy. Immunotherapy, including PD-1/PD-L1 and CTLA-4 inhibitors, shows potential, although effectiveness is constrained by the immunosuppressive tumor microenvironment and rapid progression. Targeted therapies, such as PARP inhibitors, demonstrate variable efficacy influenced by genetic heterogeneity, biomarker expression, and microenvironmental factors. Novel chemotherapeutic agents offer alternative options for cisplatin-resistant patients. Preclinical and early clinical studies suggest that combining these approaches may further enhance antitumor activity, potentially improving progression-free survival and quality of life. Biomarker-guided strategies may optimize personalized therapy and patient selection.DiscussionCisplatin resistance in SCLC arises through multiple mechanisms. First, reduction of drug deposition due to altered uptake or enhanced efflux decreases intracellular cisplatin levels. Second, dysregulation of apoptotic pathways, including overexpression of anti-apoptotic proteins such as Bcl-2, allows tumor cells to evade chemotherapy-induced cell death. Third, enhanced DNA damage repair restores cisplatin-induced lesions, limiting cytotoxicity. Fourth, the tumor microenvironment can induce resistance through stromal and immune interactions. Fifth, metabolic adaptations enable tumor cells to survive under chemotherapeutic stress. Sixth, SCLC subtype transitions alter cellular phenotype and chemosensitivity. Seventh, epigenetic changes drive transcriptional programs that confer resistance.Targeted therapies, such as multidrug resistance (MDR) inhibitors and Bcl-2 family inhibitors, can restore tumor sensitivity but are limited by toxicity and tumor-specific efficacy. Immunotherapy, including PD-1/PD-L1 and CTLA-4 inhibitors, shows potential, although effectiveness is constrained by the immunosuppressive tumor microenvironment and rapid progression. Targeted therapies, such as PARP inhibitors, demonstrate variable efficacy influenced by genetic heterogeneity, biomarker expression, and microenvironmental factors. Novel chemotherapeutic agents offer alternative options for cisplatin-resistant patients. Preclinical and early clinical studies suggest that combining these approaches may further enhance antitumor activity, potentially improving progression-free survival and quality of life. Biomarker-guided strategies may optimize personalized therapy and patient selection.ConclusionCisplatin resistance in SCLC is a complex, multifactorial process involving cellular, molecular, and microenvironmental mechanisms. Integrating mechanistic insights with emerging therapies, including immunotherapy, targeted therapy, and novel chemotherapeutics, offers a promising path to overcome resistance, guiding future research and the development of more effective, personalized treatment strategies for patients with cisplatin-resistant SCLC. 2026-12-01T00:00:00Z