Sung Goo Park

Accurately detecting disease occurrences of crops in early stage is essential for quality and yield of crops through the decision of an appropriate treatments. However, detection of disease needs specialized knowledge and long-term experiences in plant pathology. Thus, an automated system for disease detecting in crops will play an important role in agriculture by constructing early detection system of disease. To develop this system, construction of a stepwise disease detection model using images of diseased-healthy plant pairs and a CNN algorithm consisting of five pre-trained models. The disease detection model consists of three step classification models, crop classification, disease detection, and disease classification. The ‘unknown’ is added into categories to generalize the model for wide application. In the validation test, the disease detection model classified crops and disease types with high accuracy (97.09%). The low accuracy of non-model crops was improved by adding these crops to the training dataset implicating expendability of the model. Our model has the potential to apply to smart farming of Solanaceae crops and will be widely used by adding more various crops as training dataset.

Parkinson’s disease (PD) is one of the most common neurodegenerative diseases caused by the loss of dopaminergic neurons in the substantia nigra pars compacta. Although the etiology of PD is still unclear, the death of dopaminergic neurons during PD progression was revealed to be associated with abnormal aggregation of α-synuclein, elevation of oxidative stress, dysfunction of mitochondrial functions, and increased neuroinflammation. In this study, the effects of Licochalcone D (LCD) on MG132-induced neurotoxicity in primitive neural stem cells (pNSCs) derived from reprogrammed iPSCs were investigated. A cell viability assay showed that LCD had anti-apoptotic properties in MG132-induced oxidative-stressed pNSCs. It was confirmed that apoptosis was reduced in pNSCs treated with LCD through 7-AAD/Annexin Ⅴ staining and cleaved caspase3. These effects of LCD were mediated through an interaction with JunD and through the EGFR/AKT and JNK signaling pathways. These findings suggest that LCD could be a potential antioxidant reagent for preventing disease-related pathological phenotypes of PD.

Bi-Oh Park, Seong Heon Kim, Jong Hwan Kim, Seon-Young Kim, Byoung Chul Park, Sang-Bae Han, Sung Goo Park, Jeong-Hoon Kim, and Sunhong Kim. Mol. Cells 2021;44:458-67. https://doi.org/10.14348/molcells.2021.0021

Seulki Park, Kidae Kim, Keeok Haam, Hyun Seung Ban, Jung-Ae Kim, Byoung Chul Park, Sung Goo Park, Sunhong Kim & Jeong-Hoon Kim. BMB Reports 2021;54:305-10. https://doi.org/10.5483/BMBRep.2021.54.6.218

Seong Heon Kim, Jin-hwa Cho, Bi-Oh Park, Byoung Chul Park, Jeong-Hoon Kim, Sung Goo Park & Sunhong Kim. BMB Reports 2021;54:272-7. https://doi.org/10.5483/BMBRep.2021.54.5.266

Sung Ah Kim, Seung-Hyun Jo, Jin Hwa Cho, Min Yeong Yu, Ho-Chul Shin, Jung-Ae Kim, Sung Goo Park, Byoung Chul Park, Sunhong Kim, and Jeong-Hoon Kim. Mol. Cells 2020;43:935-44. https://doi.org/10.14348/molcells.2020.0122

The mammalian Target of Rapamycin (mTOR) pathway regulates a variety of physiological processes, including cell growth and cancer progression. The regulatory mechanisms of these signals are extremely complex and comprise many feedback loops. Here, we identified the deubiquitinating enzyme ovarian tumor domain-containing protein 5 (OTUD5) as a novel positive regulator of the mTOR complex (mTORC) 1 and 2 signaling pathways. We demonstrated that OTUD5 stabilized β-transducin repeat-containing protein 1 (βTrCP1) proteins via its deubiquitinase (DUB) activity, leading to the degradation of Disheveled, Egl-10, and pleckstrin domain-containing mTOR-interacting protein (DEPTOR), which is an inhibitory protein of mTORC1 and 2. We also showed that mTOR directly phosphorylated OTUD5 and activated its DUB activity. RNA sequencing analysis revealed that OTUD5 regulates the downstream gene expression of mTOR. Additionally, OTUD5 depletion elicited several mTOR-related phenotypes such as decreased cell size and increased autophagy in mammalian cells as well as the suppression of a dRheb-induced curled wing phenotype by RNA interference of Duba, a fly ortholog of OTUD5, in Drosophila melanogaster. Furthermore, OTUD5 knockdown inhibited the proliferation of the cancer cell lines with mutations activating mTOR pathway. Our results suggested a positive feedback loop between OTUD5 and mTOR signaling pathway.

Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2), regulates genes involved in cell lineage and differentiation through methylating lysine 27 on histone H3 (H3K27me3). Recurrent gain-of-function mutations of EZH2 have been identified in various cancer types, in particular, diffuse large B-cell lymphoma (DLBCL), through large-scale genome-wide association studies and EZH2 depletion or pharmacological inhibition has been shown to exert an antiproliferative effect on cancer cells, both in vitro and in vivo. In the current study, a combination of pomalidomide and GSK126 synergistically inhibited the growth of EZH2 gain-of-function mutant Diffuse large B-cell lymphoma (DLBCL) cells. Furthermore, this synergistic effect appeared to be dependent on cereblon (CRBN), a cellular receptor of pomalidomide, but not degradation of IKAROS family zinc finger 1 (IKZF1) or IKAROS family zinc finger 3 (IKZF3). RNA sequencing analyses revealed that co-treatment with GSK126 and pomalidomide induced specific gene sets involved in B-cell differentiation and apoptosis. Synergistic growth inhibition and B-cell differentiation were further validated in xenograft mouse models. Our collective results provide a molecular basis for the mechanisms underlying the combined therapeutic effects of PRC2 inhibitors and pomalidomide on EZH2-mutated DLBCL.

NF-kappa B signaling through both canonical and non-canonical pathways plays a central role in immune responses and inflammation. NF-kappa B-inducing kinase (NIK) stabilization is a key step in activation of the non-canonical pathway and its dysregulation implicated in various hematologic malignancies. The tumor suppressor, p53, is an established cellular gatekeeper of proliferation. Abnormalities of the TP53 gene have been detected in more than half of all human cancers. While the non-canonical NF-kappa B and p53 pathways have been explored for several decades, no studies to date have documented potential cross-talk between these two cancer-related mechanisms. Here, we demonstrate that p53 negatively regulates NIK in an miRNA-dependent manner. Overexpression of p53 decreased the levels of NIK, leading to inhibition of the non-canonical NF-kappa B pathway. Conversely, its knockdown led to increased levels of NIK, IKK alpha phosphorylation, and p100 processing. Additionally, miR-34b induced by nutlin-3 directly targeted the coding sequences (CDS) of NIK. Treatment with anti-miR-34b-5p augmented NIK levels and subsequent non-canonical NF-kappa B signaling. Our collective findings support a novel cross-talk mechanism between non-canonical NF-kappa B and p53.