Byung Hun Lee, Seong-Woo Bae, Jaeyoun Jay Shim, Sung Young Park, and Hye Yoon ParkMol. Cells 2016; 39(12): 841-846 https://doi.org/10.14348/molcells.2016.0277
Abstract : Local protein synthesis mediates precise spatio-temporal regulation of gene expression for neuronal functions such as long-term plasticity, axon guidance and regeneration. To reveal the underlying mechanisms of local translation, it is crucial to understand mRNA transport, localization and translation in live neurons. Among various techniques for mRNA analysis, fluorescence microscopy has been widely used as the most direct method to study localization of mRNA. Live-cell imaging of single RNA molecules is particularly advantageous to dissect the highly heterogeneous and dynamic nature of messenger ribonucleoprotein (mRNP) complexes in neurons. Here, we review recent advances in the study of mRNA localization and translation in live neurons using novel techniques for single-RNA imaging.
Namgyu Lee, and Dohoon KimMol. Cells 2016; 39(12): 847-854 https://doi.org/10.14348/molcells.2016.0310
Abstract : The early landmark discoveries in cancer metabolism research have uncovered metabolic processes that support rapid proliferation, such as aerobic glycolysis (Warburg effect), glutaminolysis, and increased nucleotide biosynthesis. However, there are limitations to the effectiveness of specifically targeting the metabolic processes which support rapid proliferation. First, as other normal proliferative tissues also share similar metabolic features, they may also be affected by such treatments. Secondly, targeting proliferative metabolism may only target the highly proliferating “bulk tumor” cells and not the slower-growing, clinically relevant cancer stem cell subpopulations which may be required for an effective cure. An emerging body of research indicates that altered metabolism plays key roles in supporting proliferation-independent functions of cancer such as cell survival within the ischemic and acidic tumor microenvironment, immune system evasion, and maintenance of the cancer stem cell state. As these aspects of cancer cell metabolism are critical for tumor maintenance yet are less likely to be relevant in normal cells, they represent attractive targets for cancer therapy.
Chan-Mi Park, Hye-Min Kim, Dong Hyun Kim, Ho-Jin Han, Haneul Noh, Jae-Hyuk Jang, Soo-Hyun Park, Han-Jung Chae, Soo-Wan Chae, Eun Kyoung Ryu, Sangku Lee, Kangdong Liu, Haidan Liu, Jong-Seog Ahn, Young Ock Kim, Bo-Yeon Kim, and Nak-Kyun SoungMol. Cells 2016; 39(12): 855-861 https://doi.org/10.14348/molcells.2016.0111
Abstract : Ginsenosides, which are the active materials of ginseng, have biological functions that include anti-osteoporotic effects. Aqueous ginseng extract inhibits osteoclast differentiation induced by receptor activator of NF-κB ligand (RANKL). Aqueous ginseng extract produces chromatography peaks characteristic of ginsenosides. Among these peaks, ginsenoside Re is a major component. However, the preventive effects of ginsenoside Re against osteoclast differentiation are not known. We studied the effect of ginsenoside Re on osteoclast differentiation, RANKL-induced tartrate-resistant acid phosphatase (TRAP) activity, and formation of multinucleated osteoclasts
Wonseok Lee, Sojin Ahn, Mengistie Taye, Samsun Sung, Hyun-Jeong Lee, Seoae Cho, and Heebal KimMol. Cells 2016; 39(12): 862-868 https://doi.org/10.14348/molcells.2016.0219
Abstract : Goats (
Xiaoyan Sun, Xueting Cai, Jie Yang, Jiao Chen, Caixia Guo, and Peng CaoMol. Cells 2016; 39(12): 869-876 https://doi.org/10.14348/molcells.2016.0023
Abstract : Cantharidin (CTD) is an active compound isolated from the traditional Chinese medicine blister beetle and displayed anticancer properties against various types of cancer cells. However, little is known about its effect on human chronic myeloid leukemia (CML) cells, including imatinib-resistant CML cells. The objective of this study was to investigate whether CTD could overcome imatinib resistance in imatinib-resistant CML cells and to explore the possible underlying mechanisms associated with the effect. Our results showed that CTD strongly inhibited the growth of both imatinib-sensitive and imatinib-resistant CML cells. CTD induced cell cycle arrest at mitotic phase and triggered DNA damage in CML cells. The ATM/ATR inhibitor CGK733 abrogated CTD-induced mitotic arrest but promoted the cytotoxic effects of CTD. In addition, we demonstrated that CTD downregulated the expression of the BCR-ABL protein and suppressed its downstream signal transduction. Real-time quantitative PCR revealed that CTD inhibited BCR-ABL at transcriptional level. Knockdown of BCR-ABL increased the cell-killing effects of CTD in K562 cells. These findings indicated that CTD overcomes imatinib resistance through depletion of BCR-ABL. Taken together, CTD is an important new candidate agent for CML therapy.
Rong-Yaun Shyu, Chun-Hua Wang, Chang-Chieh Wu, Mao-Liang Chen, Ming-Cheng Lee, Lu-Kai Wang, Shun-Yuan Jiang, and Fu-Ming TsaiMol. Cells 2016; 39(12): 877-887 https://doi.org/10.14348/molcells.2016.0161
Abstract : Tazarotene-induced gene 1 (TIG1) is a retinoic acid-inducible protein that is considered a putative tumor suppressor. The expression of TIG1 is decreased in malignant prostate carcinoma or poorly differentiated colorectal adenocarcinoma, but TIG1 is present in benign or well-differentiated tumors. Ectopic TIG1 expression led to suppression of growth in cancer cells. However, the function of TIG1 in cell differentiation is still unknown. Using a yeast two-hybrid system, we found that transmembrane protein 192 (TMEM192) interacted with TIG1. We also found that both TIG1A and TIG1B isoforms interacted and co-localized with TMEM192 in HtTA cervical cancer cells. The expression of TIG1 induced the expression of autophagy-related proteins, including Beclin-1 and LC-3B. The silencing of TMEM192 reduced the TIG1-mediated upregulation of autophagic activity. Furthermore, silencing of either TIG1 or TMEM192 led to alleviation of the upregulation of autophagy induced by all-trans retinoic acid. Our results demonstrate that the expression of TIG1 leads to cell autophagy through TMEM192. Our study also suggests that TIG1 and TMEM192 play an important role in the all-trans retinoic acid-mediated upregulation of autophagic activity.
Varun Sasidharan Nair, Mi Hye Song, Myunggon Ko, and Kwon Ik OhMol. Cells 2016; 39(12): 888-897 https://doi.org/10.14348/molcells.2016.0276
Abstract : Stable expression of Foxp3 is ensured by demethylation of CpG motifs in the
Jiyeon Ryu, Youngil Koh, Hyejoo Park, Dae Yoon Kim, Dong Chan Kim, Ja Min Byun, Hyun Jung Lee, and Sung-Soo YoonMol. Cells 2016; 39(12): 898-908 https://doi.org/10.14348/molcells.2016.0210
Abstract : Despite recent groundbreaking advances in multiple myeloma (MM) treatment, most MM patients ultimately experience relapse, and the relapse biology is not entirely understood. To define altered gene expression in MM relapse, gene expression profiles were examined and compared among 16 MM patients grouped by 12 months progression-free survival (PFS) after autologous stem cell transplantation. To maximize the difference between prognostic groups, patients at each end of the PFS spectrum (the four with the shortest PFS and four with the longest PFS) were chosen for additional analyses. We discovered that integrin-α8 (
Linh Thi Thao Nguyen, Yeon Woo Song, and Somi Kim ChoMol. Cells 2016; 39(12): 909-914 https://doi.org/10.14348/molcells.2016.0243
Abstract : Epithelial-mesenchymal transition (EMT) is a critical step in the acquisition of the migratory and invasive capabilities associated with metastatic competence. Cysteine-rich protein 61 (CCN1/Cyr61) has been implicated as an important mediator in the proliferation and metastasis of breast cancer. Hence, Cyr61 and associated pathways are attractive targets for therapeutic interventions directed against the EMT. In the present study, we report that baicalein significantly inhibits the expression of Cyr61 and migration and invasion of MDA-MB231 human breast cancer cells. Exposure to baicalein led to increased E-cadherin expression, possibly due to the ubiquitination of Snail and Slug, which was mediated by the Cyr61/Akt/glycogen synthase kinase 3β (GSK3β) pathway. Further analysis revealed that baicalein inhibited the expression of lysyl oxidase like-2 (LOXL-2), which is a functional collaborator of Snail and Slug, and subsequently attenuated the direct interaction between LOXL-2 and Snail or Slug, thereby enhancing GSK3β-dependent Snail and Slug degradation. Our findings provide new insights into the antimetastatic mechanism of baicalein and may contribute to its beneficial use in breast cancer therapies.