Evidence map›Paper›PMID 32210579›Full record

ArticleOncoTargets and therapy2020

HANR Enhances Autophagy-Associated Sorafenib Resistance Through miR-29b/ATG9A Axis in Hepatocellular Carcinoma.

Yang Shi, Xiaohua Yang, Xiaofeng Xue, Ding Sun, Peng Cai, Qingwei Song, Bin Zhang, Lei Qin

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

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  3. Progress on multifunctional transmembrane protein ATG9A.Cell communication and signaling : CCS · 2025
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  5. The role of LncRNA-mediated autophagy in cancer progression.Frontiers in cell and developmental biology · 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

8 authors at 3 institutions in 1 country.

Yang ShiDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Xiaohua YangDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Xiaofeng XueDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Ding SunDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Peng CaiDepartment of General Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, People's Republic of China.
Qingwei SongDepartment of General Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, People's Republic of China.
Bin ZhangDepartment of General Surgery, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, People's Republic of China.
Lei QinDepartment of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, People's Republic of China.
Soochow University · CNXuzhou Medical College · CNFirst Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and chemoresistance is the main obstacle for effective treatments of HCC. Accumulating studies indicated that long non-coding RNAs (lncRNAs) contribute to the chemoresistance of human carcinoma. However, the functional role of HANR in autophagy-mediated chemoresistance of HCC is unknown.

methodsThe expressions of HANR, miR-29b and ATG9A in tissues and cell lines were detected by real-time quantitative PCR (RT-qPCR). The expression of autophagy-related protein LC3-I and LC3-II was evaluated by Western blotting. The cell viability and apoptosis were examined by CCK-8 and flow cytometry, respectively. Bioinformatics analysis and luciferase activity assay were applied to determine the downstream target gene of HANR or miR-29b. Xenograft experiment was used to detect the effect of HANR on tumor growth.

resultsIn the present study, we demonstrated that HANR was notably overexpressed in sorafenib-resistant HepG2 (HepG2/sora) and sorafenib-resistant Huh7 (Huh7/sora) cells, and HANR enhanced sorafenib resistance by facilitating autophagy in HepG2/sora and Huh7/sora cells. Furthermore, we demonstrated that miR‑29b could directly interact with HANR and abolished HANR-induced sorafenib resistance by suppressing autophagy in HepG2/sora and Huh7/sora cells. Moreover, ATG9A was validated as a target of miR-29b and its overexpression obviously reversed the inhibitory effect of miR-29b on sorafenib resistance and autophagy. In addition, HANR could act as a competing endogenous RNA (ceRNA) to upregulate ATG9A expression by sponging miR-29b. Hence, HANR increased autophagy-related sorafenib resistance via inhibiting the miR-29b/ATG9A axis in HepG2/sora and Huh7/sora cells, indicating that it may be a potential target to prevent chemoresistance of HCC.

conclusionOur study revealed HANR enhanced sorafenib resistance by acting as an autophagy promoter by regulating miR-29b/ATG9A axis in sorafenib‑resistant HCC cells and might provide potential therapeutic strategies for HCC treatment.

Indexed as

ATG9AautophagyHANRHCChepatocellular carcinomamiR-29b

Identifiers

PMID32210579
PMCPMC7069583
OpenAlexW3010295291

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.