Evidence map›Paper›PMID 39641899›Full record

ArticleDigestive diseases and sciences2025

LINC01614 Accelerates CRC Progression via STAT1/LINC01614/miR-4443/PFKFB3-Mediated Aerobic Glycolysis.

Jiangyan Xia, Chenglin Zhou, Heng Zhao, Jun Zhang, Xiaoming Chai

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Article in Digestive diseases and sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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5 authors.

Jiangyan XiaDepartment of Anesthesiology, Zhongda Hospital, Southeast University, Nanjing, Jiangsu, China.
Chenglin ZhouDepartment of Anesthesiology, People's Hospital of Xuyi County, Xuyi, Huaian, Jiangsu, China.
Heng ZhaoDepartment of Anesthesiology, People's Hospital of Xuyi County, Xuyi, Huaian, Jiangsu, China.
Jun ZhangDepartment of Anesthesiology, People's Hospital of Xuyi County, Xuyi, Huaian, Jiangsu, China.
Xiaoming ChaiDepartment of Anesthesiology, People's Hospital of Xuyi County, Xuyi, Huaian, Jiangsu, China. 101008205@seu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is an aggressive malignancy among malignant tumours, with a high incidence globally. LINC01614, a long non-coding RNA, has been identified as an essential regulator in multiple cancer types. However, its biological functions and underlying molecular mechanisms in CRC remain largely unknown.

methodsIn this study, we employed RT-qPCR to assess the expression levels of LINC01614 in CRC samples. In vitro, glucose metabolism experiments were conducted to evaluate glucose metabolism in cells. The binding relationship between miR-4443, PFKFB3, and LINC01614 was confirmed through fluorescence reporter gene detection. The subcellular localization of LINC01614 in CRC cells was determined using FISH and subcellular fractionation experiments. Additionally, a mouse subcutaneous tumor model was established for in vivo experiments.

resultsOur findings reveal that LINC01614 is upregulated in CRC tissues. Silencing of LINC01614 suppresses the malignant behaviors of CRC cells, including cell proliferation, invasion, migration, and aerobic glycolysis. Furthermore, we discovered that LINC01614 promotes the expression of PFKFB3. Additional experiments demonstrated that LINC01614 binds to miR-4443, leading to the upregulation of PFKFB3 expression. Further experiments confirmed that the LINC01614/miR-4443/PFKFB3 axis promotes CRC cell malignancy by enhancing aerobic glycolysis. Additionally, we found that STAT1 promotes the transcription of LINC01614.

conclusionThese findings uncover a novel regulatory pathway wherein STAT1-induced LINC01614 enhances PFKFB3 expression by sponging miR-4443, thereby accelerating CRC development. This understanding may lead to novel therapeutic strategies for CRC treatment.

Indexed as

Colorectal NeoplasmsGlycolysisMicroRNAsPhosphofructokinase-2RNA, Long NoncodingSTAT1 Transcription FactorAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, Inbred BALB CMicroRNAsPFKFB3 protein, humanPhosphofructokinase-2RNA, Long NoncodingSTAT1 protein, humanSTAT1 Transcription FactorAerobic glycolysisColorectal cancerlncRNA

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.