Ji-Yun Seo, Ji-Hoon Kim, and Young-Yun KongMol. Cells 2019; 42(2): 97-103 https://doi.org/10.14348/molcells.2019.0004
Abstract : Androgens act in almost all tissues throughout the lifetime and have important roles in skeletal muscles. The levels of androgens increase during puberty and remain sustained at high levels in adulthood. Because androgens have an anabolic effect on skeletal muscles and muscle stem cells, these increased levels of androgens after puberty should lead to spontaneous muscle hypertrophy and hyperplasia in adulthood. However, the maintenance of muscle volume, myonuclei number per myofiber, and quiescent state of satellite cells in adulthood despite the high levels of androgens produces paradoxical outcomes. Our recent study revealed that the physiological increase of androgens at puberty initiates the transition of muscle stem cells from proliferation to quiescence by the androgen-Mindbomb1-Notch signaling axis. This newly discovered androgen action on skeletal muscles underscores the physiological importance of androgens on muscle homeostasis throughout life. This review will provide an overview of the new androgen action on skeletal muscles and discuss the paradoxical effects of androgens suggested in previous studies.
Szu-Hsien (Sam) Wu, Ji-Hyun Lee, and Bon-Kyoung KooMol. Cells 2019; 42(2): 104-112 https://doi.org/10.14348/molcells.2019.0006
Abstract : Tracking the fate of individual cells and their progeny through lineage tracing has been widely used to investigate various biological processes including embryonic development, homeostatic tissue turnover, and stem cell function in regeneration and disease. Conventional lineage tracing involves the marking of cells either with dyes or nucleoside analogues or genetic marking with fluorescent and/or colorimetric protein reporters. Both are imaging-based approaches that have played a crucial role in the field of developmental biology as well as adult stem cell biology. However, imaging-based lineage tracing approaches are limited by their scalability and the lack of molecular information underlying fate transitions. Recently, computational biology approaches have been combined with diverse tracing methods to overcome these limitations and so provide high-order scalability and a wealth of molecular information. In this review, we will introduce such novel computational methods, starting from single-cell RNA sequencing-based lineage analysis to DNA barcoding or genetic scar analysis. These novel approaches are complementary to conventional imaging-based approaches and enable us to study the lineage relationships of numerous cell types during vertebrate, and in particular human, development and disease.
Junguee Lee, Shinae Yi, Joon Young Chang, Jung Tae Kim, Hae Joung Sul, Ki Cheol Park, Xuguang Zhu, Sheue-yann Cheng, Jukka Kero, Joon Kim, and Minho ShongMol. Cells 2019; 42(2): 113-122 https://doi.org/10.14348/molcells.2018.0430
Abstract : Communications at the interface between the apical membrane of follicular cells and the follicular lumen are critical for the homeostasis of thyroid gland. Primary cilia at the apical membrane of thyroid follicular cells may sense follicular luminal environment and regulate follicular homeostasis, although their role
Nam-Ho Kim, Ali Sadra, Hee-Young Park, Sung-Min Oh, Jerold Chun, Jeong Kyo Yoon, and Sung-Oh HuhMol. Cells 2019; 42(2): 123-134 https://doi.org/10.14348/molcells.2018.0399
Abstract : Lysophosphatidic acid (LPA) is an endogenous lysophospholipid with signaling properties outside of the cell and it signals through specific G protein-coupled receptors, known as LPA1?6. For one of its receptors, LPA1 (gene name
Sang-Hun Choi, Jun-Kyum Kim, Hee-Young Jeon, Kiyoung Eun, and Hyunggee KimMol. Cells 2019; 42(2): 135-142 https://doi.org/10.14348/molcells.2018.0311
Abstract : OCT4, also known as POU5F1 (POU domain class 5 transcription factor 1), is a transcription factor that acts as a master regulator of pluripotency in embryonic stem cells and is one of the reprogramming factors required for generating induced pluripotent stem cells. The human OCT4 encodes three isoforms, OCT4A, OCT4B, and OCT4B1, which are generated by alternative splicing. Currently, the functions and expression patterns of OCT4B remain largely unknown in malignancies, especially in human glioblastomas. Here, we demonstrated the function of OCT4B in human glioblastomas. Among the isoform of OCT4B, OCT4B-190 (OCT4B19kDa) was highly expressed in human glioblastoma stem cells and glioblastoma cells and was mainly detected in the cytoplasm rather than the nucleus. Overexpression of OCT4B19kDa promoted colony formation of glioblastoma cells when grown in soft agar culture conditions. Clinical data analysis revealed that patients with gliomas that expressed OCT4B at high levels had a poorer prognosis than patients with gliomas that expressed OCT4B at low levels. Thus, OCT4B19kDa may play a crucial role in regulating cancer cell survival and adaption in a rigid environment.
Zhongwei Wang, Wei Mei, Qingde Wang, Rundong Guo, Peilin Liu, Yuqiang Wang, Zijuan Zhang, and Limin WangMol. Cells 2019; 42(2): 143-150 https://doi.org/10.14348/molcells.2018.0028
Abstract : Chronic neuropathic pain is one of the primary causes of disability subsequent to spinal cord injury. Patients experiencing neuropathic pain after spinal cord injury suffer from poor quality of life, so complementary therapy is seriously needed. Dehydrocorybulbine is an alkaloid extracted from
Kyoung-Jin Lee, Kyeong Han Park, and Jang-Hee HahnMol. Cells 2019; 42(2): 151-160 https://doi.org/10.14348/molcells.2018.0423
Abstract : Ultraviolet (UV) radiation of the sunlight, especially UVA and UVB, is the primary environmental cause of skin damage, including topical inflammation, premature skin aging, and skin cancer. Previous reports show that activation of nuclear factor-κB (NF-κB) in human skin fibroblasts and keratinocytes after UV exposure induces the expression and release of proinflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α), and subsequently leads to the production of matrix metalloproteases (MMPs) and growth factor basic fibroblast growth factor (bFGF). Here, we demonstrated that TNFR2-SKEE and TNFR2-SKE, oligopeptides from TNF receptor-associated factor 2 (TRAF2)-binding site of TNF receptor 2 (TNFR2), strongly inhibited the interaction of TNFR1 as well as TNFR2 with TRAF2. In particular, TNFR2-SKE suppressed UVB- or TNF-α-induced nuclear translocalization of activated NF-κB in mouse fibroblasts. It decreased the expression of bFGF, MMPs, and COX2, which were upregulated by TNF-α, and increased procollagen production, which was reduced by TNF-α. Furthermore, TNFR2-SKE inhibited the UVB-induced proliferation of keratinocytes and melanocytes in the mouse skin and the infiltration of immune cells into inflamed tissues. These results suggest that TNFR2-SKE may possess the clinical potency to alleviate UV-induced photoaging in human skin.
Yangki Seok, Won Kee Lee, Jae Yong Park, and Dong Sun KimMol. Cells 2019; 42(2): 161-165 https://doi.org/10.14348/molcells.2018.0322
Abstract : Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related deaths worldwide and has high rates of metastasis. Transforming growth factor beta-inducible protein (TGFBI) is an extracellular matrix component involved in tumour growth and metastasis. However, the exact role of TGFBI in NSCLC remains controversial. Gene silencing via DNA methylation of the promoter region is common in lung tumorigenesis and could thus be used for the development of molecular biomarkers. We analysed the methylation status of the
Hanhae Kim, Anna Joe, Muyoung Lee, Sunmo Yang, Xiaozhi Ma, Pamela C. Ronald, and Insuk LeeMol. Cells 2019; 42(2): 166-174 https://doi.org/10.14348/molcells.2018.0403
Abstract : Bacterial species in the genus
Hoin Kang, Chongtae Kim, Eunbyul Ji, Sojin Ahn, Myeongwoo Jung, Youlim Hong, WooK Kim, and Eun Kyung LeeMol. Cells 2019; 42(2): 175-182 https://doi.org/10.14348/molcells.2018.0288
Abstract : microRNAs regulate a diverse spectrum of cancer biology, including tumorigenesis, metastasis, stemness, and drug resistance. To investigate miRNA-mediated regulation of drug resistance, we characterized the resistant cell lines to 5-fluorouracil by inducing stable expression of miRNAs using lenti-miRNA library. Here, we demonstrate miR-551a as a novel factor regulating cell survival after 5-FU treatment. miR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation. It was further shown that myocyte-specific factor 2C is the direct target of miR-551a. Our results suggest that miR-551a plays a novel function in regulating 5-FU-induced cell death, and targeting miR-551a might be helpful to sensitize cells to anti-cancer drugs.