• Journal of Microbiology and Biotechnology
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• 제31권10호
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• pp.1358-1365
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• 2021

To clarify the role of long intergenic nonprotein-coding RNA 1232 (LINC01232) in the progression of gastric cancer and the potential mechanism, we analyzed the expression of LINC01232 in TCGA database using the GEPIA online tool, and the LINC01232 level in gastric cancer cell lines was detected by quantitative real time-polymerase chain reaction (qRT-PCR) as well. Cell proliferation assay, colony formation assay, transwell assay and tumor formation experiment in nude mice were conducted to observe the biological behavior changes of gastric cancer cells through the influence of LINC01232 knockdown. LncATLAS database and subcellular isolation assay were used for subcellular distribution of LINC01232 in gastric cancer cells. The interaction among LINC01232, zeste homolog 2 (EZH2) and kruppel-like factor 2 (KLF2) was clarified by RNA-protein interaction prediction (RPISeq), RNA immunoprecipitation (RIP), qRT-PCR and chromatin immunoprecipitation (ChIP) assay. Rescue experiments were further conducted to elucidate the biological function of LINC01232/KLF2 axis in the progression of gastric cancer. LINC01232 was upregulated in stomach adenocarcinoma (STAD) tissues and gastric cancer lines. LINC01232 knockdown inhibited the proliferative capacities of gastric cancer cells in vitro, and impaired in vivo tumorigenicity. LINC01232 was mainly distributed in the cell nucleus where it epigenetically repressed KLF2 expression via binding to the enhancer of EZH2, which was capable of binding to promoter regions of KLF2 to induce histone H3 lysine 27 trimethylation (H3K27me3). LINC01232 exerts oncogenic activities in gastric cancer via inhibition of KLF2, and therefore, the knockdown of KLF2 could reverse the regulatory effect of LINC01232 in the proliferative ability of gastric cancer cells.

• Journal of Microbiology and Biotechnology
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• 제31권7호
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• pp.921-932
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• 2021

LINC01272 is a long non-coding RNA (lncRNA) that has been considered as a biomarker for many diseases including lung squamous cell carcinoma. Here, we investigated the function and mechanism of LINC01272 on lung cancer (LC). The differential expression of LINC01272 in LC and normal samples was analyzed by GEPIA based on the data from TCGA-LUAD database, as survival prognosis was analyzed through Kaplan-Meier Plotter. LINC01272 overexpression plasmid and miR-7-5p mimic were transfected into A549 and PC-9 cells. LINC01272, miR-7-5p and cardiolipin synthase 1 (CRLS1) mRNA expression was measured by quantitative reverse transcription-polymerase chain reaction. Cell viability was detected through MTT assay. Cell multiplication was evaluated by cell formation assay. Cell apoptosis was assessed through flow cytometry assay. Through bioinformatics, the target miRNA of LINC01272 and downstream genes of miR-7-5p were predicted. The targeting relationship was tested by dual luciferase reporter analysis. CRLS1, B-cell lymphoma-2 (Bcl-2), BCL2-associated X (Bax) and cleaved caspase-3 protein levels were detected through western blot. LINC01272 was downregulated in LC and low LINC01272 expression had poor prognosis. In A549 and PC-9 cells, LINC01272 inhibited cell viability and multiplication and induced apoptosis. LINC01272 negatively regulated miR-7-5p and CRLS1 was a target of miR-7-5p. MiR-7-5p reversed the effect of LINC01272 on viability, multiplication, apoptosis and expression of miR-7-5p and CRLS1 as well as apoptosis-related factors (Bcl-2, Bax and cleaved caspase-3). LINC01272 suppressed cell multiplication and induced apoptosis via regulating the miR-7-5p/CRLS1 axis in LC.

• Journal of Microbiology and Biotechnology
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• 제33권3호
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• pp.398-409
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• 2023

LncRNAs play crucial roles in the progression of colon adenocarcinoma (COAD), but the role of LINC01232 in COAD has not received much attention. The present study was designed to explore the related mechanisms of LINC01232 in the progression of COAD. LINC01232, miR-181a-5p, p53, c-myc, Bcl-2, cyclin D1, p16, Bax, VEGF, E-cadherin, vimentin, N-cadherin and SDAD1 expressions were determined by western blot and qRT-PCR. CCK-8, tubule formation, and Transwell assays were employed to detect proliferation, angiogenesis, and migration/invasion of COAD cells, respectively. The relationship between LINC01232 and miR-181a-5p was predicted by LncBase Predicted v.2, and then verified through dual luciferase reporter gene assay. According to the results, LINC01232 was highly expressed in COAD cells and enhanced proliferation, angiogenesis, migration, and invasion of COAD cells. Downregulated LINC01232 promoted expression of p53 and p16, and inhibited c-myc, Bcl-2 and cyclin D1 expressions in COAD cells, while upregulation of LINC01232 generated the opposite effects. LINC01232 was negatively correlated with miR-181a-5p while downregulated miR181a-5p could reverse the effects of siLINC01232 on cell proliferation, angiogenesis, migration, and invasion. Similarly, miR-181a-5p mimic could also offset the effect of LINC01232 overexpression. SiLINC01232 increased the expressions of Bax and E-cadherin, and decreased the expressions of VEGF, vimentin, N-cadherin and SDAD1, which were partially attenuated by miR-181a-5p inhibitor. Collectively, LINC01232 enhances the proliferation, migration, invasion, and angiogenesis of COAD cells by decreasing miR-181a-5p expression.

• 한국산학기술학회논문지
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• 제17권1호
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• pp.605-614
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• 2016

2012년부터 실무적인 교육 훈련을 촉진시키기 위해 정부로부터 많은 대학이 산학협력선도대학(LINC) 사업을 활발히 적용해왔으며, 주로 기술혁신형 프로그램과 현장밀착형 프로그램으로 구분된다. Fishbein과 Azjen에 의해 주장된 계획행동이론은 마케팅, 친환경구매, 기술 등과 같은 영역에서 행동의도를 예측하기 위해 연구되었으나 산학협력과 관련하여 이를 적용한 연구는 부족한 실정이다. 본 연구의 목적은 계획행동이론을 적용하여 기업 실무자의 산학협력 참여의도 및 행동을 실증적으로 검증하는 것이며, 총 32개의 설문문항을 바탕으로 132개의 데이터 중 115개를 연구에 활용하였다. 본 연구의 구체적인 결과는 다음과 같다. 태도, 주관적 규범, 지각된 행동통제는 LINC사업 참여의도에 유의한 예측변수로 나타났으며, LINC 사업 참여는 LINC 사업 참여 행동에 유의한 예측변수임을 실증적으로 확인하였다.

• Journal of Microbiology and Biotechnology
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• 제31권8호
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• pp.1098-1108
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• 2021

The literature indicates that LINC00174 promotes the growth of colorectal cancer (CRC) cells, but its research needs to be enriched. We tried to explore the function and mechanism of LINC00174 in CRC cell proliferation and migration. Bioinformatics analysis predicted the binding relationship and expressions of lncRNA, miRNA and mRNA. Clinical study analyzes the relationship between LINC00174 and clinical data characteristics of CRC patients. The expressions of LINC00174, miR-3127-5p and E2F7 were verified by RT-qPCR, and the combination of the two was verified by dual luciferase analysis and RNA immunoprecipitation as needed. Western blot was used to detect the expression of EMT-related protein and E2F7 protein. Functional experiments were used to evaluate the function of the target gene on CRC cells. LINC00174 was up-regulated in CRC clinical samples and cells and was related to the clinical characteristics of CRC patients. High-expression of LINC00174, contrary to the effect of siLINC00174, promoted cell viability, proliferation, migration and invasion, up-regulated the expressions of N-Cadherin, Vimentin, E2F7, and inhibited the expression of E-Cadherin. MiR-3127-5p was one of the targeted miRNAs of LINC00174 and was down-regulated in CRC samples. In addition, miR-3127-5p mimic partially reversed the malignant phenotype of CRC cells induced by LINC00174. Besides, E2F7 was a target gene of miR-3127-5p, and LINC00174 repressed miR-3127-5p to regulate E2F7. Our research reveals that LINC00174 affected the biological characteristics of CRC cells through regulated miR-3127-5p/ E2F7 axis.

• Journal of Gastric Cancer
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• 제19권4호
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• pp.460-472
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• 2019

Purpose: Long noncoding RNA 00703 (LINC00703) was found originating from a region downstream of Kruppel-like factor 6 (KLF6) gene, having 2 binding sites for miR-181a. Since KLF6 has been reported as a target of miR-181a in gastric cancer (GC), this study aims to investigate whether LINC00703 regulates the miR-181a/KLF6 axis and plays a functional role in GC pathogenesis. Materials and Methods: GC tissues, cell lines, and nude mice were included in this study. RNA binding protein immunoprecipitation (RIP) and pull-down assays were used to evaluate interaction between LINC00703 and miR-181a. Quantitative real-time polymerase chain reaction and western blot were applied for analysis of gene expression at the transcriptional and protein levels. A nude xenograft mouse model was used to determine LINC00703 function in vivo. Results: We revealed that LINC00703 competitively interacts with miR-181a to regulate KLF6. Overexpression of LINC00703 inhibited cell proliferation, migration/invasion, but promoted apoptosis in vitro, and arrested tumor growth in vivo. LINC00703 expression was found to be decreased in GC tissues, which was positively correlated with KLF6, but negatively with the miR-181a levels. Conclusions: LINC00703 may have an anti-cancer function via modulation of the miR-181a/KLF6 axis. This study also provides a new potential diagnostic marker and therapeutic target for GC treatment.

• The Korean Journal of Physiology and Pharmacology
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• 제27권3호
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• pp.197-208
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• 2023

Dysregulation of certain long non-coding RNAs may facilitate tumor initiation and progression. However, numerous carcinogenesis-related long noncoding RNAs have not been characterized. The goal of this study was to elucidate the role of LINC00562 in gastric cancer (GC). The expression of LINC00562 was analyzed using real-time quantitative PCR and Western blotting. The proliferative capacity of GC cells was determined using Cell Counting Kit-8 and colony-formation assays. The migration of GC cells were evaluated using wound-healing assays. The apoptosis of GC cells was assessed by measuring the expression levels of apoptosis-related proteins (Bax and Bcl-2). Xenograft models in nude mice were constructed for in vivo functional analysis of LINC00562. The binding relationship between miR-4636 and LINC00562 or adaptor protein complex 1 sigma 3 (AP1S3), obtained from public databases, was confirmed using dual-luciferase and RNA-binding protein immunoprecipitation experiments. LINC00562 was expressed in GC cells at high levels. Knockdown of LINC00562 repressed GC cell growth and migration, promoted apoptosis in vitro, and inhibited tumor growth in nude mouse models. LINC00562 directly targeted miR-4636, and miR-4636 depletion restored the GC cell behavior inhibited by LINC00562 absence. AP1S3, an oncogene, binds to miR-4636. MiR-4636 downregulation increased AP1S3 level, restoring GC cell malignant behaviors inhibited by AP1S3 downregulation. Thus, LINC00562 exerts carcinogenic effects on GC development by targeting miR-4636-mediated AP1S3 signaling.

• 한국전자파학회논문지
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• 제19권5호
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• pp.547-555
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• 2008

본 논문에서는 linear amplification with nonlinear components(LINC) 시스템의 두 신호 경로에 발생하는 크기와 위상 오차를 자동으로 검출하여 보상하는 알고리즘을 제안하였다. LINC 시스템은 첨두 대 평균 전력비가 큰 non-constant envelop 신호를 constant envelop 신호로 바꿔주어 고효율 전력 증폭기를 사용할 수 있는 장점이 있다. 그러나 LINC 시스템은 두 전력 증폭기의 경호에서 발생하는 매우 작은 경로 오차에 민감하게 성능이 열화된다는 단점이 있다. 본 논문에서는 4개의 테스트 신호를 이용하여 두 경로의 크기와 위상 오차를 검출하는 알고리즘을 제안하였다. 제안된 오차 검출 기법은 닫힌 해(closed form solution)를 가지며, 반복 계산이 필요하지 않아, 빠르고 효율적으로 오차를 검출할 수 있다. 본 논문에서는 제안된 기법을 적용하여 오차 검출과 검출된 결과를 반영하여 신호의 왜곡을 보상하는 digital-IF 형태를 갖는 LINC 시스템을 구현하였다. 구현된 LINC 시스템은 7 MHz 채널 대역을 갖고 16-QAM으로 변조된 IEEE 802.16 WiMAx 기저 대역 신호를 이용하여 성능을 분석하였으며, 제안된 기법을 이용하여 EVM이 -37.37 dB까지 개선되었으며, 이로서 LINC 시스템 구현시 제안된 오차 검출 및 보상 기법의 적용 타당성을 확인하였다.

• 한국산학기술학회논문지
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• 제18권7호
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• pp.175-183
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• 2017

본 연구는 LINC사업이 종료되고 새롭게 시행되는 LINC+(사회맞춤형 산학협력 선도대학)이 새롭게 시작되는 시점에서 LINC+사업의 핵심 어젠더인 대학과 산업체의 쌍방향 산학협력이 정착되기 위해서 대학 중심의 성과측정 외에 산업체입장에서 고려되어야 할 요소를 발견하고자 한다. 기업의 입장에서 기업의 매출액 증가, 고용증가. 수출 증가 등의 양적인 성과요인도 있지만 산학협력의 결과로 어느 정도의 기업에 기여하고 있는지를 측정하기가 쉽지 않다. 따라서 산학협력의 만족도를 측정함과 동시에 이러한 만족도 요인이 기업의 입장에서 실제 성장 발전에 미치는 기여도를 동시에 측정함으로써 산학협력 프로그램의 만족도가 기업의 성장발전에 기여하는 정도를 주관적 지표를 통해 측정하고자 하는 것이다. 이를 통해 LINC+사업 시행으로 추진하고자 하는 "산업선도형 대학" 육성을 통한 사회수요 맞춤형 인재양성, 산학협력을 기반으로 하는 중소기업 혁신 지원 및 일자리 창출, 일관성 있는 산학협력 지원을 통해 정부 정책의 신뢰도 제고로 대학과 산업체의 상생발전에 조력하고자한다.

• 한국지역지리학회지
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• 제21권4호
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• pp.649-659
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• 2015

2011년부터 시행된 교육과학기술부의 LINC 사업을 통해 산학협력중점교수 제도가 처음 도입된 이후, 산학협력중점교수의 수는 가파르게 증가하였고, 산학협력 활동의 매개 주체로서 산학협력중점교수가 중요한 역할을 수행하고 있는 것으로 평가되고 있다. 그러나 산학협력중점교수 제도 운영에 필요한 인건비의 70%를 LINC 사업비에 의존하고 있는 프로젝트 사업의 특성상 LINC 사업에서 중도 탈락하거나 LINC 사업이 종료된 후에도 산학협력중점교수 제도가 존속할 수 있을지 의문이 제기되고 있는 상황이다. 이에 본 연구에서는 문헌고찰을 비롯해 산학협력중점교수 제도를 운영하고 있는 대학들을 대상으로 한 설문조사 및 전문가 심층면담조사 결과를 토대로 산학협력중점교수의 실태 및 문제점을 파악하였다. 그리고 이를 바탕으로 제도 개선방안을 법 제도적, 재정적, 구조적인 측면에서 제시하였다.