Evidence map›Paper›PMID 33499874›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3.

Gege Shu, Huizhao Su, Zhiqian Wang, Shihui Lai, Yan Wang, Xiaomeng Liu, Luo Dai, Yin Bi, Wei Chen, Weiyu Huang and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 61 citations in OpenAlex.

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  7. GABPA-Mediated Expression of HPN-AS1 Facilitates Cell Apoptosis and Inhibits Cell Proliferation in Hepatocellular Carcinoma by Promoting eIF4A3 Degradation.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Gege Shu *Department of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Huizhao Su *Department of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Zhiqian Wang *Department of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Shihui LaiDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Yan WangDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Xiaomeng LiuDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Luo DaiDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Yin BiDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Wei ChenDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Weiyu HuangDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Ziyan ZhouDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China.
Songqing HeDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China. Dr_hesongqing@163.com.
Hongliang DaiDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China. jy2006hldai@sohu.com.
Bo TangDepartment of Hepatobiliary Surgery, Key Laboratory of Basic and Clinical Application Research for Hepatobiliary Diseases, The First Affiliated Hospital of Guangxi Medical University, No. 6 Shuangyong Road, Nanning, 530021, Guangxi, People's Republic of China. dr_sntangbo@163.com.
Guangxi Medical University · CNFirst Affiliated Hospital of GuangXi Medical University · CN

Funding

National Natural Science Foundation of China 81700519National Natural Science Foundation of China 81871938
6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) has an extremely poor prognosis due to the development of chemoresistance, coupled with inherently increased stemness properties. Long non-coding RNAs (LncRNAs) are key regulators for tumor cell stemness and chemosensitivity. Currently the relevance between LINC00680 and tumor progression was still largely unknown, with only one study showing its significance in glioblastoma. The study herein was aimed at identifying the role of LINC00680 in the regulation HCC stemness and chemosensitivity.

methodsQRT-PCR was used to detect the expression of LINC00680, miR-568 and AKT3 in tissue specimen and cell lines. Gain- or loss-of function assays were applied to access the function of LINC00680 in HCC cells, including cell proliferation and stemness properties. HCC stemness and chemosensitivity were determined by sphere formation, cell viability and colony formation. Luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to examine the interaction between LINC00680 and miR-568 as well as that between miR-568 and AKT3. A nude mouse xenograft model was established for the in vivo study.

resultsWe found that LINC00680 was remarkably upregulated in HCC tissues. Patients with high level of LINC00680 had poorer prognosis. LINC00680 overexpression significantly enhanced HCC cell stemness and decreased in vitro and in vivo chemosensitivity to 5-fluorouracil (5-Fu), whereas LINC00680 knockdown led to opposite results. Mechanism study revealed that LINC00680 regulated HCC stemness and chemosensitivity through sponging miR-568, thereby expediting the expression of AKT3, which further activated its downstream signaling molecules, including mTOR, elF4EBP1, and p70S6K.

conclusionLINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3, suggesting that LINC00680 might be a potentially important HCC diagnosis marker and therapeutic target.

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAnimalsBiomarkers, TumorCarcinoma, HepatocellularCell Line, TumorComputational BiologyDrug Resistance, NeoplasmFemaleGene Expression ProfilingHumansLiver NeoplasmsMaleMiceMicroRNAsAKT3 protein, humanBiomarkers, TumorMicroRNAsMIRN568 microRNA, humanProto-Oncogene Proteins c-aktRNA, Long NoncodingAKT3ChemosensitivityHepatocellular carcinomaLINC00680miR-568Stemness

Identifiers

PMID33499874
PMCPMC7836199
OpenAlexW3122593695

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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.