Evidence map›Paper›PMID 35426224›Full record

ArticleJournal of cellular and molecular medicine2022

ASIC1a stimulates the resistance of human hepatocellular carcinoma by promoting EMT via the AKT/GSK3β/Snail pathway driven by TGFβ/Smad signals.

Yinci Zhang, Niandie Cao, Jiafeng Gao, Jiaojiao Liang, Yong Liang, Yinghai Xie, Shuping Zhou, Xiaolong Tang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 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

8 authors.

Yinci ZhangMedcial School, Anhui University of Science & Technology, Huainan, China.ORCID 0000-0003-1925-8557
Niandie CaoMedcial School, Anhui University of Science & Technology, Huainan, China.
Jiafeng GaoMedcial School, Anhui University of Science & Technology, Huainan, China.
Jiaojiao LiangMedcial School, Anhui University of Science & Technology, Huainan, China.
Yong LiangInstitute of Environment-friendly Materials and Occupational Health of Anhui, University of Science and Technology, Wuhu, China.
Yinghai XieMedcial School, Anhui University of Science & Technology, Huainan, China.
Shuping ZhouMedcial School, Anhui University of Science & Technology, Huainan, China.
Xiaolong TangMedcial School, Anhui University of Science & Technology, Huainan, China.

Funding

Anhui Provincial Science and Technology program 1604a0802094Anhui Provincial Science and Technology program 202004j07020053Research Foundation of the Institute of Environment-friendly Materials and Occupational Health (Wuhu), Anhui University of Science and Technology ALW2020YF11The National Natural Science Fund of China 81572431The National Natural Science Fund of China 81872017The National Natural Science Fund of China 82071862University Natural Science Research Project of Anhui Province KJ2018A0097University Natural Science Research Project of Anhui Province KJ2018ZD011University Natural Science Research Project of Anhui Province KJ2019A0093University Natural Science Research Project of Anhui Province KJ2020A0340
6 · The paper itself

Abstract

Multidrug resistance is the main obstacle to curing hepatocellular carcinoma (HCC). Acid-sensing ion channel 1a (ASIC1a) has critical roles in all stages of cancer progression, especially invasion and metastasis, and in resistance to therapy. Epithelial to mesenchymal transition (EMT) transforms epithelial cells into mesenchymal cells after being stimulated by extracellular factors and is closely related to tumour infiltration and resistance. We used Western blotting, immunofluorescence, qRT-PCR, immunohistochemical staining, MTT, colony formation and scratch healing assay to determine ASIC1a levels and its relationship to cell proliferation, migration and invasion. ASIC1a is overexpressed in HCC tissues, and the amount increased in resistant HCC cells. EMT occurred more frequently in drug-resistant cells than in parental cells. Inactivation of ASIC1a inhibited cell migration and invasion and increased the chemosensitivity of cells through EMT. Overexpression of ASIC1a upregulated EMT and increased the cells' proliferation, migration and invasion and induced drug resistance; knocking down ASIC1a with shRNA had the opposite effects. ASIC1a increased cell migration and invasion through EMT by regulating α and β-catenin, vimentin and fibronectin expression via the AKT/GSK-3β/Snail pathway driven by TGFβ/Smad signals. ASIC1a mediates drug resistance of HCC through EMT via the AKT/GSK-3β/Snail pathway.

Indexed as

Acid Sensing Ion ChannelsCarcinoma, HepatocellularEpithelial-Mesenchymal TransitionLiver NeoplasmsCell Line, TumorCell MovementGlycogen Synthase Kinase 3 betaHumansProto-Oncogene Proteins c-aktSignal TransductionSnail Family Transcription FactorsTransforming Growth Factor betaAcid Sensing Ion ChannelsASIC1 protein, humanGlycogen Synthase Kinase 3 betaProto-Oncogene Proteins c-aktSnail Family Transcription FactorsTransforming Growth Factor betaacid-sensing ion channel 1aAKT/GSK-3β/Snail pathwaychemosensitivityepithelial to mesenchymal transitionhepatocellular carcinomainvasionmigrationmultidrug resistance

Identifiers

PMID35426224
PMCPMC9097844

What OpenQuestion holds

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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.