Evidence map›Paper›PMID 31802650›Full record

Observational studyCancer medicine2020

LncRNA NEAT1 knockdown attenuates autophagy to elevate 5-FU sensitivity in colorectal cancer via targeting miR-34a.

Fen Liu, Fei-Yan Ai, De-Cai Zhang, Li Tian, Zhen-Yun Yang, Shao-Jun Liu

Open access · goldAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

67 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
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  7. Circular RNA-Encoded Proteins in Disease Pathogenesis.International journal of biological sciences · 2025
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  11. Translational cancer research · 2024
    Article
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7 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Fen LiuDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, P.R. China.
Fei-Yan AiDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, P.R. China.
De-Cai ZhangDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, P.R. China.
Li TianDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, P.R. China.
Zhen-Yun YangDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, P.R. China.
Shao-Jun LiuDepartment of Gastroenterology, The Third Xiangya Hospital of Central South University, Changsha, P.R. China.ORCID 0000-0001-5374-1302
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundsColorectal carcinoma (CRC) is a common malignant tumor. Increasing evidences indicated that CRC showed a resistance to 5-fluorouracil (5-FU) and further resulted in a poor prognosis. In this study, we aim to investigate the effect of long noncoding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) on cell viability, sensitivity to 5-FU, and autophagy of CRC cell lines.

methodsMTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-Htetrazolium bromide) was used to detect cell viability, immunofluorescent staining was used to detect autophagy puncta, and luciferase reporter system was used to determine binding ability between miR-34a and NEAT1 or putative targets. Additionally, indicated mRNAs and protein expressions were determined by qRT-PCR or western blotting, respectively.

resultsWe found that NEAT1 expression was increased in CRC tissues and cells, which showed a negative correlation with miR-34a expression. In addition, NEAT1 knockdown noticeably inhibited the proliferation of CRC cells and enhanced 5-FU sensitivity. It revealed that NEAT1 knockdown suppressed the LC3 puncta and the expressions of Beclin-1, ULK1, and ratio of LC3II/I. Overexpression of miR-34a showed similar trends with NEAT1 knockdown. miR-34a was validated to target the putative binding sites in 3'-UTR of HMGB1, ATG9A, and ATG4B, which are involved in the activation of autophagy. Inhibition of miR-34a or overexpression of HMGB1 could effectively reverse elevated 5-FU sensitivity upon NEAT1 knockdown. In addition, 3-MA reversed NEAT1 overexpression-induced resistance in HT29 cells.

conclusionThese findings indicate that LncRNA NEAT1 could target miR-34a and promote autophagy to facilitate 5-FU chemoresistance in CRC.

Indexed as

3' Untranslated RegionsApoptosisAutophagyAutophagy-Related ProteinsCell ProliferationCell SurvivalColorectal NeoplasmsCysteine EndopeptidasesDrug Resistance, NeoplasmFluorouracilGene Expression Regulation, NeoplasticGene Knockdown TechniquesHMGB1 ProteinHT29 CellsHumansMembrane Proteins3' Untranslated RegionsATG4B protein, humanATG9A protein, humanAutophagy-Related ProteinsCysteine EndopeptidasesFluorouracilHMGB1 ProteinHMGB1 protein, humanMembrane ProteinsMicroRNAsMIRN34 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingVesicular Transport Proteinsautophagycolorectal carcinomaHMGB1LncRNA NEAT1miR-34a

Identifiers

PMID31802650
PMCPMC6997058
OpenAlexW2992758483

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.