Bonsang Koo, Baekgyu Choi, Hoewon Park, and Ki-Jun YoonMol. Cells 2019; 42(9): 617-627
Abstract : Brain organoids are an exciting new technology with the potential to significantly change our understanding of the development and disorders of the human brain. With step-by-step differentiation protocols, three-dimensional neural tissues are self-organized from pluripotent stem cells, and recapitulate the major millstones of human brain development
Chaobing Ma, Xueyin Zu, Kangdong Liu, Ann M. Bode, Zigang Dong, Zhenzhen Liu, and Dong Joon KimMol. Cells 2019; 42(9): 628-636 https://doi.org/10.14348/molcells.2019.0038
Abstract : Altered genetic features in cancer cells lead to a high rate of aerobic glycolysis and metabolic reprogramming that is essential for increased cancer cell viability and rapid proliferation. Pyruvate kinase muscle (PKM) is a rate-limiting enzyme in the final step of glycolysis. Herein, we report that PKM is a potential therapeutic target in triple-negative breast cancer (TNBC) cells. We found that PKM1 or PKM2 is highly expressed in TNBC tissues or cells. Knockdown of PKM significantly suppressed cell proliferation and migration, and strongly reduced S phase and induced G2 phase cell cycle arrest by reducing phosphorylation of the CDC2 protein in TNBC cells. Additionally, knockdown of PKM significantly suppressed NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity by reducing the phosphorylation of p65 at serine 536, and also decreased the expression of NF-κB target genes. Taken together, PKM is a potential target that may have therapeutic implications for TNBC cells.
Kieu Thi Xuan Vo, Sang-Kyu Lee, Morgan K. Halane, Min-Young Song, Trung Viet Hoang, Chi-Yeol Kim, Sook-Young Park, Junhyun Jeon, Sun Tae Kim, Kee Hoon Sohn, and Jong-Seong JeonMol. Cells 2019; 42(9): 637-645 https://doi.org/10.14348/molcells.2019.0070
Abstract : Effector-triggered immunity (ETI) is an effective layer of plant defense initiated upon recognition of avirulence (Avr) effectors from pathogens by cognate plant disease resistance (R) proteins. In rice, a large number of
Quy Thi Cam Nguyen, Sun-ji Lee, Seo-wha Choi, Yeon-ju Na, Mi-ran Song, Quyen Thi Ngoc Hoang, Seo Young Sim, Min-Sik Kim, Jeong-Il Kim, Moon-Soo Soh, and Soo Young KimMol. Cells 2019; 42(9): 646-660 https://doi.org/10.14348/molcells.2019.0173
Abstract : Abscisic acid (ABA) is a phytohormone essential for seed development and seedling growth under unfavorable environmental conditions. The signaling pathway leading to ABA response has been established, but relatively little is known about the functional regulation of the constituent signaling components. Here, we present several lines of evidence that Arabidopsis Raf-like kinase Raf10 modulates the core ABA signaling downstream of signal perception step. In particular, Raf10 phosphorylates subclass III SnRK2s (SnRK2.2, SnRK2.3, and SnRK2.6), which are key positive regulators, and our study focused on SnRK2.3 indicates that Raf10 enhances its kinase activity and may facilitate its release from negative regulators. Raf10 also phosphorylates transcription factors (ABI5, ABF2, and ABI3) critical for ABA-regulted gene expression. Furthermore, Raf10 was found to be essential for the
Jianming Hua, Ning Shen, Jingkai Wang, Yiqing Tao, Fangcai Li, Qixin Chen, and Xiaopeng ZhouMol. Cells 2019; 42(9): 661-671 https://doi.org/10.14348/molcells.2019.0098
Abstract : Adipose tissue-derived mesenchymal stem cells (ADSCs) are promising for regenerating degenerated intervertebral discs (IVDs), but the low efficiency of nucleus pulposus (NP)-specific differentiation limits their clinical applications. The Sonic hedgehog (Shh) signaling pathway is important in NP-specific differentiation of ADSCs, and Smoothened Agonist (SAG) is a highly specific and effective agonist of Shh signaling. In this study, we proposed a new differentiation strategy with the use of the small molecule SAG. The NP-specific differentiation and extracellular matrix (ECM) synthesis of ADSCs were measured
Jae Hyun Kwon, Jooyoung Lee, Jiye Kim, Varvara A. Kirchner, Yong Hwa Jo, Takeshi Miura, Nayoung Kim, Gi-Won Song, Shin Hwang, Sung-Gyu Lee, Young-In Yoon, and Eunyoung TakMol. Cells 2019; 42(9): 672-685 https://doi.org/10.14348/molcells.2019.0003
Abstract : Currently, liver transplantation is the only available remedy for patients with end-stage liver disease. Conservation of transplanted liver graft is the most important issue as it directly related to patient survival. Carbonyl reductase 1 (CBR1) protects cells against oxidative stress and cell death by inactivating cellular membrane-derived lipid aldehydes. Ischemia-reperfusion (I/R) injury during living-donor liver transplantation is known to form reactive oxygen species. Thus, the objective of this study was to investigate whether CBR1 transcription might be increased during liver I/R injury and whether such increase might protect liver against I/R injury. Our results revealed that transcription factor Nrf2 could induce CBR1 transcription in liver of mice during I/R. Pre-treatment with sulforaphane, an activator of Nrf2, increased CBR1 expression, decreased liver enzymes such as aspartate aminotransferase and alanine transaminase, and reduced I/R-related pathological changes. Using oxygen-glucose deprivation and recovery model of human normal liver cell line, it was found that oxidative stress markers and lipid peroxidation products were significantly lowered in cells overexpressing CBR1. Conversely, CBR1 knockdown cells expressed elevated levels of oxidative stress proteins compared to the parental cell line. We also observed that Nrf2 and CBR1 were overexpressed during liver transplantation in clinical samples. These results suggest that CBR1 expression during liver I/R injury is regulated by transcription factor Nrf2. In addition, CBR1 can reduce free radicals and prevent lipid peroxidation. Taken together, CBR1 induction might be a therapeutic strategy for relieving liver I/R injury during liver transplantation.