• 천문학회보
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• 제44권2호
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• pp.68.1-68.1
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• 2019

Turbulence plays a crucial role in controlling star formation as it produces density fluctuation as well as non-thermal pressure against gravity. Therefore, turbulence controls the mode and tempo of star formation. However, despite a plenty of previous studies, the properties of turbulence remain poorly understood. As part of the Taeduk Radio Astronomy Observatory (TRAO) Key Science Program (KSP), "mapping Turbulent properties In star-forming MolEcular clouds down to the Sonic scale (TIMES; PI: Jeong-Eun Lee)", we mapped the Orion A and the Ophiuchus clouds, in three sets of lines (13CO 1-0/C18O 1-0, HCN 1-0/HCO+ 1-0, and CS 2-1/N2H+ 1-0) with a high-velocity resolution (~0.1 km/s) using the TRAO 14-m telescope. The mean Trms for the observed maps are less than 0.25 K, and all these maps show uniform Trms values throughout the observed area. These homogeneous and high signal-to-noise ratio data provide the best chance to probe the nature of turbulence in two different star-forming clouds, the Orion A and Ophiuchus clouds. We present comparisons between the line intensities of different molecular tracers as well as the results of a Principal Component Analysis (PCA).

• Biomolecules & Therapeutics
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• 제32권1호
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• pp.123-135
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• 2024

Although gemcitabine-based regimens are widely used as an effective treatment for pancreatic cancer, acquired resistance to gemcitabine has become an increasingly common problem. Therefore, a novel therapeutic strategy to treat gemcitabine-resistant pancreatic cancer is urgently required. Piceamycin has been reported to exhibit antiproliferative activity against various cancer cells; however, its underlying molecular mechanism for anticancer activity in pancreatic cancer cells remains unexplored. Therefore, the present study evaluated the antiproliferation activity of piceamycin in a gemcitabine-resistant pancreatic cancer cell line and patient-derived pancreatic cancer organoids. Piceamycin effectively inhibited the proliferation and suppressed the expression of alpha-actinin-4, a gene that plays a pivotal role in tumorigenesis and metastasis of various cancers, in gemcitabine-resistant cells. Long-term exposure to piceamycin induced cell cycle arrest at the G₀/G₁ phase and caused apoptosis. Piceamycin also inhibited the invasion and migration of gemcitabine-resistant cells by modulating focal adhesion and epithelial-mesenchymal transition biomarkers. Moreover, the combination of piceamycin and gemcitabine exhibited a synergistic antiproliferative activity in gemcitabine-resistant cells. Piceamycin also effectively inhibited patient-derived pancreatic cancer organoid growth and induced apoptosis in the organoids. Taken together, these findings demonstrate that piceamycin may be an effective agent for overcoming gemcitabine resistance in pancreatic cancer.

• Molecules and Cells
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• 제37권12호
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• pp.873-880
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• 2014

In our previous study, miRNA-183, a miRNA in the miR-96-182-183 cluster, was significantly over-expressed in esophageal squamous cell carcinoma (ESCC). In the present study, we explored the oncogenic roles of miR-183 in ESCC by gain and loss of function analysis in an esophageal cancer cell line (EC9706). Genome-wide mRNA micro-array was applied to determine the genes that were regulated directly or indirectly by miR-183. 3'UTR luciferase reporter assay, RT-PCR, and Western blot were conducted to verify the target gene of miR-183. Cell culture results showed that miR-183 inhibited apoptosis (p < 0.05), enhanced cell proliferation (p < 0.05), and accelerated G1/S transition (p < 0.05). Moreover, the inhibitory effect of miR-183 on apoptosis was rescued when miR-183 was suppressed via miR-183 inhibitor (p < 0.05). Western blot analysis showed that the expression of programmed cell death 4 (PDCD4), which was predicted as the target gene of miR-183 by microarray profiling and bioinformatics predictions, decreased when miR-183 was over-expressed. The 3'UTR luciferase reporter assay confirmed that miR-183 directly regulated PDCD4 by binding to sequences in the 3'UTR of PDCD4. Pearson correlation analysis further confirmed the significant negative correlation between miR-183 and PDCD4 in both cell lines and in ESCC patients. Our data suggest that miR-183 might play an oncogenic role in ESCC by regulating PDCD4 expression.

• Molecules and Cells
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• 제38권2호
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• pp.130-137
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• 2015

MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3'-UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3'-UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.

• Molecules and Cells
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• 제41권5호
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• pp.423-435
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• 2018

This investigation was aimed at working out the combined role of lncRNA H19, miR-29b and Wnt signaling in the development of colorectal cancer (CRC). In the aggregate, 185 CRC tissues and corresponding para-carcinoma tissues were gathered. The human CRC cell lines (i.e. HT29, HCT116, SW480 and SW620) and normal colorectal mucosa cell line (NCM460) were also purchased. Si-H19, si-NC, miR-29b-3p mimics, miR-29b-3p inhibitor, si-PGRN and negative control (NC) were, respectively, transfected into the CRC cells. Luciferase reporter plasmids were prepared to evaluate the transduction activity of $Wnt/{\beta}-catenin$ signaling pathway, and dual-luciferase reporter gene assay was arranged to confirm the targeted relationship between H19 and miR-29b-3p, as well as between miR-29b-3p and PGRN. Finally, the proliferative and invasive capacities of CRC cells were appraised through transwell, MTT and scratch assays. As a result, overexpressed H19 and down-expressed miR-29b-3p displayed close associations with the CRC patients' poor prognosis (P < 0.05). Besides, transfection with si-H19, miR-29b-3p mimic or si-PGRN were correlated with elevated E-cadherin expression, decreased snail and vimentin expressions, as well as less-motivated cell proliferation and cell metastasis (P < 0.05). Moreover, H19 was verified to directly target miR-29b-3p based on the luciferase reporter gene assay (P < 0.05), and miR-29b-3p also bound to PGRN in a direct manner (P < 0.05). Finally, addition of LiCl ($Wnt/{\beta}-catenin$ pathway activator) or XAV93920 ($Wnt/{\beta}-catenin$ pathway inhibitor) would cause remarkably altered E-cadherin, c-Myc, vimentin and snail expressions, as well as significantly changed transcriptional activity of ${\beta}-catenin/Tcf$ reporter plasmid (P < 0.05). In conclusion, the lncRNA H19/miR-29b-3p/PGRN/Wnt axis counted a great deal for seeking appropriate diagnostic biomarkers and treatment targets for CRC.

• Elastomers and Composites
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• 제40권4호
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• pp.277-283
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• 2005

주사슬에 옥텐을 각각 15.3, 17.0 mol% 함유하고 있는 $PEO_{15},\;PEO_{17}$과 시클로알칸으로 이루어진 2성분계 혼합물이 단일상에서 액상과 기상으로 분리되는 LV 곡선을 측정하였다. ($PEO_{15}$+시클로펜탄) 용액이 액상과 기상으로 분리되는 압력이 ($PEO_{17}$+시클로펜탄)의 경우보다 약 $1.1{\sim}2.7$ bar 높게 측정되었다. ($PEO_{17}$+시클로헥산)의 경우, LV 곡선이 ($PEO_{15}$+시클로헥산) LV 곡선보다 $0.9{\sim}l.6$ bar 낮은 압력에서 측정되었다. 수평균 분자량이 82,200인 $PEO_{15}$보다 분자량이 1.9배 큰 $PEO_{17}$과 시클로알칸으로 구성된 용액의 LV 곡선 압력이 ($PEO_{15}$+ 시클로알칸) 용액의 LV 곡선 압력보다 낮은 것은 $PEO_{15}$와 $PEO_{17}$ 사이의 옥텐반복기의 함량차이로 인한 PEO 사슬구조의 차이 때문이다. $PEO_{15}$와 $PEO_{17}$에 함유된 옥텐반복기의 차이가 1.7mole%로 매우 작으나, 이 작은 옥텐반복기 함량차이가 PEO 용액의 LV 곡선 압력에 차이를 줄 정도로 상거동에 크게 영향을 준다.

• Radiation Oncology Journal
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• 제16권4호
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• pp.377-388
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• 1998

목적 : 방사선조사에 의한 apoptosis에서 나타나는 각종 세포주기관련 유전자들의 발현 양상을 RNA와 단백 수준에서 분석하여 방사선조사에 의한 apoptosis에서의 세포주기 조절의 변화를 규명함으로서 방사선치료의 기전에 대한 분자생물학적 이해를 도모하고자 본 연구를 시행하였다. 대상 및 방법 : promyelocytic leukemia 세포주인 HL60 세포주를 배양하여 선형가속기(6MV X-선)로 세포에 8Gy의 방사선을 조사하였다. 조사후 다양한 시간 간격으로 Apoptotic DNA Fragmentation Assay법을 이용하여 apoptosis를 확인하고 동시에 세포주기관련 유전자들(cyclinA, cyclin B, cyclin C, cyclin Dl, cyclin E, cdc2, CDK2, CDK4, $p16^{INK4a}$, $p21^{WAF1}$, $p27^{KIP1}$, E2F, PCNA와 Rb)을 단백질과 RNA 수준에서 분석하기위해 western blot analysis와 반정량적 RT-PCR을 시행하였다. 결과: 8 Gy의 방사선 조사에 의해 HL60세포에서 apoptosis가 관찰 되었다. 방사선 조사군에서 cyclin A단백은 조사후 48시간까지 시간이 갈수록 증가하였으며, cyclin E, E2F, CDK2 및 Rb 단백은 증가되었다가 다시 감소를 보였다. Rb단백의 증가는 대부분 비활성형인 ppRb (phosphorylated Rb protein)의 양적변화에 의한 것이었다. cyclin Dl, PCNA, COC2, CDK4, $p16^{INK4a}$단백은 발현의 차이를 보이지 않았으며 $p21^{WAF1}$과 $p27^{KIP1}$ 단백은 검출되지 않았다. cyclin A, B, C mRNA는 방사선 조사 직후 감소하였다가 12시간부터 발현이 증가되었으며 cyclin Dl mRNA는 조사후 바로 증가하여 48시간에 다시 감소하였다. cyclin E mRNA는 조사 후 시간이 경과함에 따라 감소하였다. CDK2 mRNA는 3시간째는 감소하다가 6시간부터 많은 증가를 보였으며 CDK4 mRNA는 조사후 6-12시간에 급격한 발현증가를 보였다. $p16^{INK4a}$ RNA는 발현의 변화가 없었으며, $p21^{WAF1}$ 및 $p27^{KIP1}$ RNA의 발현은 관찰되지 않았다. 결론 : 이상의 결과로 미루어볼 때, 방사선 조사에 의한 HL60세포의 apoptosis와 세포의 Gl/S transition는 밀접한 관계가 있는 것으로 생각되며 Rb단백의 증가와 활성형 Rb단백의 감소 현상도 관련이 있는 것으로 사료된다. 이는 E2F의 비정상적인 과발현 및 cyclin E/CDK2의 발현 증가와 관련이 있는 것으로 추측된다. 또한 $p21^{WAF1}$ 및 $p27^{KIP1}$는 방사선에 의한 apoptosis에는 관여되지 않는 것으로 사료된다.

• 생명과학회지
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• 제29권6호
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• pp.679-687
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• 2019

본 연구에서는 인체 폐암 세포인 A549를 사용하여 Litsea populifolia 에탄올 추출물(EELP)의 항산화 및 항암활성과 그 분자적 기전에 관하여 연구하였다. 먼저 EELP의 DPPH 라디칼 소거활성을 측정한 결과, $IC_{50}$가 $11.71{\mu}g/ml$로 유의적인 항산화활성을 보였다. 또한 EELP가 인체폐암세포주인 A549와 정상 폐세포인 IMR90의 세포증식에 미치는 영향을 알아본 결과, 정상세포의 생존율에는 거의 영향을 끼치지 않은 반면, EELP 농도의존적으로 A549 세포의 성장이 저해되었으며, 세포 주기 변화를 분석한 결과 EELP에 의해 A549 세포의 강력한 G1 arrest가 유도되는 것을 확인하였다. EELP에 의해 유도되는 G1 arrest는 세포주기 조절 인자인 Cyclin D1, Cyclin E, Cyclin-dependent kinase인 CDK2와 CDK6의 mRNA 발현 감소와 더불어 단백질 발현 감소와 연관되어 있었다. 또한 EELP 처리에 의한 CDK/Cyclin complex의 발현 저해는 DNA 손상에 의해 활성화되는 CHK2의 활성화 형태인 p-CHK2의 발현 증가에 따른 p53 인산화에 따른 활성화와 CDK 활성화 효소인 CDC25A 탈인산화효소의 인산화에 따른 저해에 의해 나타나는 결과로 사료된다. 이러한 결과들로부터 EELP는 두가지 경로인 p53-의존성과 p53-비의존성(ATM/CHK2/CDC25A/CDK2) 경로를 통해 A549의 G1 arrest를 유도하여 세포 증식을 억제하는 것으로 사료된다. 본 연구결과는 EELP가 폐암에 대한 새로운 항암활성 소재로서 사용될 수 있는 가능성을 시사하며, 또한 EELP의 세포주기 조절에 의한 항암기전을 이해하고 향후 지속적 연구를 하는 데 있어서 귀중한 기초자료로 사용될 수 있을 것이다.