Evidence map›Paper›PMID 32324343›Full record

ArticleCancer medicine2020

SNGH16 regulates cell autophagy to promote Sorafenib Resistance through suppressing miR-23b-3p via sponging EGR1 in hepatocellular carcinoma.

Zhao Jing, Xiaoping Ye, Xiaojie Ma, Xiangrong Hu, Wenjun Yang, Junping Shi, Gongying Chen, Ling Gong

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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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 2 institutions in 1 country.

Zhao JingDepartment of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, China.
Xiaoping YeDepartment of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Xiaojie MaDepartment of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Xiangrong HuDepartment of Pathology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Wenjun YangDepartment of Pathology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Junping ShiDepartment of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Gongying ChenDepartment of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.
Ling GongDepartment of Liver Diseases, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, China.ORCID 0000-0002-4446-2165
Affiliated Hospital of Hangzhou Normal University · CNHangzhou Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTumor cells could acquire drug resistance through cell autophagy. This study aimed to explore the role of SNHG16 in sorafenib-resistant HCC cells and its mechanism with miR-23b-3p.

methodsThe sorafenib-resistant Hep3B cell model was established. The SNHG16 and miR-23b-3p gene expressions were determined in normal HCC and sorafenib-resistant HCC tissues. Detection of the expression of SNHG16 and miR-23b-3p and its respective correlation with survival rate were performed. Target genes to SNHG16 and miR-23b-3p were predicted, and verified by dual-fluorescent reporter assay. The effects of SNHG16 and miR-23b-3p on SNHG16, miR-23b-3p, EGR1 expression, viability, apoptosis as well as LC3II/LC3 expression in Hep3B and Hep3B/So cells were detected by qRT-PCR, CCK-8, flow cytometry, and western blot. In in vivo studies, the NOD/SCID mice model was established to explore the effects of Hep3B and Hep3B/So cells with inhibited SNHG16 or miR-23b-3p on tumor size, EGR1 expression, and autophagy.

resultsHigh SNHG16 expression in HCC-resistant tissues and low miR-23b-3p expression in all HCC tissues were detected, and the two were negatively correlated. Low SNHG16 and high miR-23b-3p were related to a high survival rate of HCC patients. Moreover, SNHG16 overexpression promoted Hep3B/So cell viability and autophagy, suppressed apoptosis by inhibiting miR-23b-3p expression through up-regulating EGR1, however, the effect of si-SNHG16 was opposite. In in vivo studies, miR-23b-3p inhibitor suppressed the high sorafenib sensitivity in Hep3B/So cells caused by SNHG16 silencing through promoting viability, autophagy, and suppressing apoptosis.

conclusionSNHG16 promotes Hep3B/So cell viability, autophagy, and inhibits apoptosis to maintain its resistance to sorafenib through regulating the expression of miR-23b-3p via sponging EGR1.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCarcinoma, HepatocellularCell ProliferationEarly Growth Response Protein 1HumansLiver NeoplasmsMaleMiceMice, Inbred NODMice, SCIDMicroRNAsPrognosisAntineoplastic AgentsBiomarkers, TumorEarly Growth Response Protein 1EGR1 protein, humanMicroRNAsMIRN23b microRNA, humanRNA, Long NoncodingSNHG16 lncRNA, humanSorafenibEGR1hepatocellular carcinomaMiR-23b-3pSNHG16sorafenib resistance

Identifiers

PMID32324343
PMCPMC7300419
OpenAlexW3020609753

What OpenQuestion holds

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LicenceCC BY
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.