LINC01232 Promotes Gastric Cancer Proliferation through Interacting with EZH2 to Inhibit the Transcription of KLF2

( Jing Liu ),( Zhen Li ),( Guohua Yu ),( Ting Wang ),( Guimei Qu ),( Yunhui Wang ) 한국미생물 · 생명공학회 2021 Journal of microbiology and biotechnology Vol.31 No.10

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.

LINC01272 Suppressed Cell Multiplication and Induced Apoptosis Via Regulating MiR-7-5p/CRLS1 Axis in Lung Cancer

( Xuan Ma ),( Yang Liu ),( Hao Tian ),( Bo Zhang ),( Meiling Wang ),( Xia Gao ) 한국미생물생명공학회(구 한국산업미생물학회) 2021 Journal of microbiology and biotechnology Vol.31 No.7

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.

전문대학 LINC 사업의 정책효과 분석

오상기(Oh, Sangki),권순형(Kwon Soon Hyoung),이윤식(Lee Yun Sik),박주현(Park, Joohyun),안병훈(Ahn, Byunghun),문영빛(Moon, Youngbit) 한국교육행정학회 2018 敎育行政學硏究 Vol.36 No.1

본 연구는 전문대학 LINC사업의 성과를 분석하는 데 주된 목적을 두고 있다. 이를 위해 본 연구는 경향점수매칭(Propensity Score Matching) 방법을 활용하여 사업 선정 과정에서 활 용된 성과지표를 성과 변인으로 설정하여 전문대학 LINC 사업을 수혜 받은 대학과 비 수혜 대학 간 비교․분석하였다. 본 연구의 주요 결과를 요약하면 다음과 같다. 첫째, 경향점수 매칭 전 성과 변인은 사업을 수행한 대학이 보다 높게 나타났으나, 경향점 수매칭 후 분석결과에서는 산학협력단 수익률과 산업체 경력교수 비율만 통계적으로 의미가 있었다. 둘째, 전문대학 LINC 사업의 선정 과정에서 학교규모는 통계적으로 의미가 있는 영 향 변인으로 파악되었다. 셋째, 정책성과 변인 가운데 산출 변인으로 파악될 수 있는 취업률, 현장실습 이수율, 창업지원 강의 이수 학생비율과 같은 변인은 사업 수혜대학과 비 수혜대학 간 통계적으로 차이가 없었다. 이와 같은 내용을 토대로 전문대학 LINC 사업의 1단계 사업 종료 시점의 성과 변인을 활용하여 본 사업의 정책효과를 분석했다는 점에서 의미는 있지만, 정책의 영향에 대한 평가를 포괄하지 않는다는 점에서 종단자료를 활용하여 전문대학 산학협 력 전반에 대한 종합적인 정책평가가 필요함을 제언하였다. The purpose of this study is to analyze the achievements of the College’LINC project of south korea. The policy analysis was used as the propensity score matching (PSM) method and independent t-test between LINC project and non-LINC project colleges. The main results of this study are summarized as follows. First, the achivement score was higher in the LINC school that performed the project than non-LINC school. However, in the analysis results after the propensity score matching, only two variables (industry-Academia Collaboration Foundations’s revenue and industry professorship’s ratio) were statistically significant. Second, the school size was found to be a statistically significant influential variable in the process of selecting the LINC project of the college. Third, the variables such as the employment rate, field practice rate, and the ratio of students attending the start - up support lecture were not statistically different between the LINC college and non-LINC college. Based on the above, We discussed the policy effects of the LINC project and suggested some points to consider in the process of the LINC project.

Upregulated Long Noncoding RNA LINC01234 Predicts Unfavorable Prognosis for Colorectal Cancer and Negatively Correlates With KLF6 Expression

Xiao Jiang,Qiaoying Zhu,Pengxi Wu,Fengsheng Zhou,Jun Chen 대한진단검사의학회 2020 Annals of Laboratory Medicine Vol.40 No.2

Background: LINC01234, a long noncoding RNA (lncRNA), is overexpressed in several cancers, including colorectal cancer (CRC). We investigated the role of LINC01234 in CRC development and confirmed its correlation with Krüppel-like factor 6 (KLF6), a tumor suppressor gene that is dysregulated in CRC. Methods: We tested mRNA levels using quantitative reverse transcription PCR (qRT-PCR). Tissue samples from patients with CRC, inflammatory bowel disease (IBD), hyperplastic polyp, and adenoma were included. Correlations between clinicopathological parameters, overall survival (OS) rate, and LINC01234 were analyzed using Kruskal-Wallis H test. Additionally, cell proliferation, apoptosis, and tumor formation in nude mice were tested to investigate the mechanism of LINC01234. Western blotting was used to determine protein levels. Results: LINC01234 expression was significantly upregulated in CRC tissues and CRC cell lines than in non-tumor tissues and normal epithelial cells, respectively. LINC01234 was associated with high tumor stage, larger tumor size, and metastasis. Patients with higher LINC01234 expression showed reduced OS. Cell proliferation was inhibited by LINC01234 knockdown, whereas apoptosis was enhanced. Mice injected with SW480 cells with LINC01234 knockdown displayed decreased tumor volume, weight, and Ki-67 levels compared with those injected with control cells. KLF6 was negatively regulated by LINC01234. Overexpression of KLF6 showed effects similar to those observed following LINC01234 knockdown on cell proliferation and apoptosis. Conclusions: LINC01234 could be a prognostic biomarker in CRC patients. Upregulation of LINC01234 in CRC promotes tumor development through negative regulation of KLF6.

예산집행 유형에 따른 LINC+ 참여 대학 간 산학협력 성과 차이 분석

김훈호(Hoonho Kim),김영식(Young-sik Kim) 한국교육재정경제학회 2022 敎育財政 經濟硏究 Vol.31 No.3

본 연구는 2017년부터 2019년까지 3년 동안 산학협력 고도화형 LINC+ 사업에 참여한 50개 일반대학들을 대상으로 이들의 예산 집행 유형과 이에 따른 산학협력 성과 차이를 분석하였다. 이를 위하여 우선 각대학의 항목별 예산 집행 비율에 대한 군집분석을 실시한 결과, LINC+ 참여 대학들의 예산 집행 유형을‘산학협력 관련 교육프로그램 및 기업 연계 집중형’과 ‘산학협력 인프라 집중형’의 두 가지로 구분하였다. 이와 함께 LINC+ 참여 대학들의 예산 집행 유형에 따른 산학협력 성과 차이를 분석한 결과, ‘산학협력인프라 집중형’ 대학들의 ‘계약학과 재학생 비율‘이 ‘교육프로그램 및 기업 연계 집중형’ 대학들에 비해 높은 것으로 나타난 반면, 기타 종속변수들에서는 예산 집행 유형에 따른 산학협력 성과 차이가 나타나지않음을 확인하였다. 본 연구는 위의 분석 결과를 통해 LINC 3.0의 경우 사업 예산 편성 및 집행에 대한 대학의 자율성을확대할 필요가 있으며, 효과적인 사업비 집행 및 성과 제고를 위한 대학 및 정책당국의 지원이 필요함을정책적 시사점으로 제안하였다. 이와 함께 LINC+ 사업의 산학협력 성과에 대한 보다 면밀한 분석과 함께이에 기반한 정책 수정 및 보완 노력이 지속적으로 이루어질 필요가 있음을 추가적으로 제안하였다. This research aimed to empirically investigate the types of LINC+ budget execution of individual universities participated in LINC+ and the industry-university cooperation performance differences based on the derived budget execution types, and to suggest policy implications to improve the performance of LINC 3.0. To achieve the purpose, this study exploits LINC+ budget execution dataset of 50 universities participated in LINC+ from 2017 to 2019 utilizing cluster analysis, OLS and fixed effect model. The major findings showed that LINC+ budget execution can be divided into ‘Industry-university cooperative program and industry linkage centered universities’ and ‘Industry-university cooperative infrastructure centered universities’. Furthermore, ‘infrastructure-centered universities’ were more effective in improving the ratio of students involved in contract department with industry than ‘program and industry-linkage centered universities’. This study attempted to provide useful policy implications to improve the performance of individual universities participated in LINC 3.0 and suggestions for policy practitioners in the field of industry-university cooperation.

LncRNA LINC00313 Knockdown Inhibits Tumorigenesis and Metastasis in Human Osteosarcoma by Upregulating FOSL2 through Sponging miR-342-3p

Hongtao Chen,Paerhati Wahafu,Leilei Wang,Xuan Chen 연세대학교의과대학 2020 Yonsei medical journal Vol.61 No.5

Purpose: Osteosarcoma (OS) is the most common primary bone tumor, with high morbidity in infants and adolescents. Long noncoding RNA LINC00313 has been found to modulate papillary thyroid cancer tumorigenesis and to be dysregulate in lung cancer. However, the role of LINC00313 in OS has not yet been addressed. Materials and Methods: We evaluated mRNA and protein expression using real-time quantitative PCR and Western blotting. Cell proliferation was evaluated using MTT; apoptosis and autophagy were assessed with flow cytometry, Western blotting, and/or GFP-LC3 assay. Transwell assay was conducted to measure cell migration and invasion. Potential target sites for LINC00313 and miR-342-3p were predicted with starBase v.2.0 and TargetScan Human, and verified using luciferase reporter assay, RNA immunoprecipitation, and RNA pull-down assay. In vivo, xenogeneic tumors were induced with U2OS and MG-63 cells, separately. Results: LINC00313 was upregulated and miR-342-3p was downregulated in OS tissues and cells. High expression of LINC00313 was associated with shorter overall survival. FOSL2 downregulation and miR-342-3p overexpression suppressed cell proliferation and migratory and invasive abilities while promoting apoptosis and autophagy, all of which were consistent with the effects of LINC00313 knockdown. miR-342-3p, sponged by LINC00313, inversely modulated FOSL2 by targeting MG-63 cells, and FOSL2 expression was positively controlled by LINC00313. LINC00313 knockdown suppressed tumor growth in vivo. Conclusion: LINC00313 is upregulated in OS, and LINC00313 knockdown plays a vital anti-tumor role in OS cell progression through a miR-342-3p/FOSL2 axis. Our study suggests that LINC00313 may be a novel, promising biomarker for diagnosis and prognosis of OS.

LncRNA linc01194 promotes the progress of endometrial carcinoma by up-regulating SOX2 through binding to IGF2BP1

Zhenghao Huang,Fan Shen,Jingwen Chen,Bumin Xie,Xi Chen,Yang Zhao,Shuo Chen 대한부인종양학회 2024 Journal of Gynecologic Oncology Vol.35 No.2

Objective: Endometrial carcinoma (EC) is one of the most common gynecological malignanttumors. Our study showed that long non-coding RNA (lncRNA) linc01194 plays an importantrole in EC. We explored the mechanism of lncRNA linc01194 in EC. Methods: The expression of lncRNA linc01194 was detected in The Cancer Genome Atlasdatabase and starBase database. The potential targeted protein of linc01194 was predictedthrough the starBase database. To determine the role of linc01194 in EC, we downregulatedor upregulated the level of linc01194 in EC cell lines and analyzed the cell behaviors and thechanges of its potential target proteins. Results: The expression of linc01194 in EC tissues is higher than that in normal endometrialtissues. The knockdown of linc01194 inhibited the cell proliferation, invasion and migrationand promoted the apoptosis of EC cells, while overexpression of linc01194 promoted cellproliferation, invasion and migration and inhibited the apoptosis of EC cells. The starBasedatabase revealed that linc01194 could bind to insulin-like growth factor 2 binding protein 1(IGF2BP1). Previous results showed that in EC, IGF2BP1 could promote the expression of sex-determining region Y-box 2 (SOX2) by promoting the stability of SOX2 mRNA. Our resultsshowed that linc01194 regulate the expression of IGF2BP1 and SOX2. Conclusion: Linc01194 can promote the expression of downstream protein SOX2 throughbinding to IGF2BP1, thus promoting the occurrence and development of EC.

LINC00174 Facilitates Proliferation and Migration of Colorectal Cancer Cells via MiR-3127-5p/ E2F7 Axis

( Yuhong Ma ),( Yuzhen Li ),( Yuanyuan Tang ),( Ning Tang ),( Dengke Wang ),( Xiaofei Li ) 한국미생물 · 생명공학회 2021 Journal of microbiology and biotechnology Vol.31 No.8

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.

LncRNA LINC01232 Enhances Proliferation, Angiogenesis, Migration and Invasion of Colon Adenocarcinoma Cells by Downregulating miR-181a-5p

( Yu Yuan ),( Zhou Long ) 한국미생물생명공학회 2023 Journal of microbiology and biotechnology Vol.33 No.3

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 miR-181a-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.

LINC00657 knockdown suppresses hepatocellular carcinoma progression by sponging miR-424 to regulate PD-L1 expression

Xinling Cao,Guanping Zhang,Tao Li,Chengming Zhou,Lei Bai,Jinming Zhao,Turgunjan Tursun 한국유전학회 2020 Genes & Genomics Vol.42 No.11

Background Hepatocellular carcinoma (HCC) is the sixth most commonly diagnosed malignant tumor and the fourth leadingcause of cancer-related deaths worldwide. As a novel non-coding RNA, LINC00657 was firstly identified as an oncogenicrole in breast cancer. However, few research focus on the effect of LINC00657 on the progression of HCC. Objectives The purpose of this study was to investigate the effect of LINC00657 on HCC tissues and cells, and furtherexplore the potential mechanism. Methods We first measured the expression of LINC00657 in HCC tissues and cell lines using qRT-PCR. Next we establishedLINC00657 knockdown in HCC cells. CCK-8 assay, cell invasion assay, flow cytometry analysis, qRT-PCR and westernblotting were applied to assess the role of LINC00657 knockdown in the biological behavior of HCC cells. The bioinformaticsanalysis and the rescue experiment were devoted to the underlying mechanism. Results LINC00657 was remarkably overexpressed in HCC tissues and cell lines, associated with poor prognosis. LINC00657knockdown repressed cell proliferation and invasion, promoted cell apoptosis of HCC cell lines. The bioinformatics analysisshowed LINC00657 sponged miR-424 as a ceRNA. Besides, PD-L1 mimic rescued the suppression of si-LINC00657 inthe biological behavior of HCC cells. Conclusion In a word, we observed LINC00657 regulated PD-L1 expression by sponging miR-424, thus affecting the developmentsof hepatocellular carcinoma. These findings LINC00657 may provide new evidence for therapeutic application inhepatocellular carcinoma.