Evidence map›Paper›PMID 38992207›Full record

ArticleFunctional & integrative genomics2024

TGF-β1-Induced LINC01094 promotes epithelial-mesenchymal transition in hepatocellular carcinoma through the miR-122-5p/TGFBR2-SAMD2-SMAD3 Axis.

Xiaofeng Yang, Cuicui Xu, Chenghao Liu, Xiangwei Wu, Xueling Chen, Jun Hou, Lianghai Wang

Abstract read
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In one paragraph

Article in Functional & integrative genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

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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

7 authors.

Xiaofeng Yang *NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China.
Cuicui Xu *NHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China.
Chenghao LiuNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China.
Xiangwei WuNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China.
Xueling ChenNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China.
Jun HouNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China. houjun229@163.com.
Lianghai WangNHC Key Laboratory of Prevention and Treatment of Central Asia High Incidence Diseases, Shihezi University, Shihezi, Xinjiang, China. lh_wang@shzu.edu.cn.

Funding

Bingtuan Science and Technology Program 2021BC002National Natural Science Foundation of China 82360503Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences 2020-PT330-003
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis. It has been proven that long non-coding RNAs (lncRNAs) play an essential role in regulating HCC progression. However, the involvement of LINC01094 in regulating epithelial-mesenchymal transition (EMT) in HCC remains unclear. LINC01094 expression in HCC patients was retrieved from the Cancer Genome Atlas database. Overexpressing and downregulating LINC01094 were conducted to investigate its biological functions using Hep3B, SNU-387, and HuH-7 cells. Western blotting and morphological observation were performed to study the EMT in HCC cells. Transwell assay was adopted to determine the migration and invasion of HCC cells. The underlying mechanism of competitive endogenous RNAs (ceRNAs) was investigated using bioinformatics analysis, quantitative reverse-transcription polymerase chain reaction, and rescue experiments. Elevated LINC01094 expression was observed in HCC and associated with a poor prognosis. Knockdown of LINC01094 expression in SNU-387 and HuH-7 cells could inhibit migration, invasion, and EMT markers. Overexpression of LINC01094 indicated that LINC01094 promoted EMT via the TGF-β/SMAD signaling pathway. The bioinformatics analysis revealed that miR-122-5p was a target of LINC01094. The miRWalk database analysis showed that TGFBR2, SMAD2, and SMAD3 were downstream targets of miR-122-5p. Mechanically, LINC01094 acted as a ceRNA that facilitated HCC metastasis by sponging miR-122-5p to regulate the expression of TGFBR2, SMAD2, and SMAD3. Further, TGF-β1 could enhance the expression of LINC01094, forming a positive feedback loop. TGF-β1-induced LINC01094 expression promotes HCC cell migration and invasion by targeting the miR-122-5p/TGFBR2-SMAD2-SMAD3 axis. LINC01094 may be a potential prognostic biomarker and therapeutic target for HCC metastasis.

Indexed as

Carcinoma, HepatocellularEpithelial-Mesenchymal TransitionLiver NeoplasmsMicroRNAsReceptor, Transforming Growth Factor-beta Type IIRNA, Long NoncodingSmad3 ProteinTransforming Growth Factor beta1Cell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansSignal TransductionMicroRNAsMIRN122 microRNA, humanReceptor, Transforming Growth Factor-beta Type IIRNA, Long NoncodingSmad3 ProteinSMAD3 protein, humanTGFB1 protein, humanTGFBR2 protein, humanTransforming Growth Factor beta1EMTHCCMetastasismiR-122-5pTGF-β1

Identifiers

PMID38992207

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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.