Evidence map›Paper›PMID 37937948›Full record

ArticleCell cycle (Georgetown, Tex.)2023

SNHG15 promotes gallbladder cancer progression by enhancing the autophagy of tumor cell under nutrition stress.

He Min, Linhua Yang, Xinsen Xu, Yajun Geng, Fatao Liu, Yingbin Liu

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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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

6 authors at 3 institutions in 1 country.

He MinState Key Laboratory of Oncogenes and Related Genes, Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Linhua YangState Key Laboratory of Oncogenes and Related Genes, Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Xinsen XuState Key Laboratory of Oncogenes and Related Genes, Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Yajun GengState Key Laboratory of Oncogenes and Related Genes, Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Fatao LiuShanghai Cancer Institute, State Key Laboratory of Oncogenes and Related Genes, Shanghai, China.
Yingbin LiuState Key Laboratory of Oncogenes and Related Genes, Department of Biliary-Pancreatic Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
State Key Laboratory of Oncogene and Related Genes · CNShanghai Jiao Tong University · CNShanghai Cancer Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gallbladder cancer (GBC) is a major malignant carcinoma of the biliary tract with extremely poor prognosis. Currently, there is no useful therapy strategies for GBC treatment, indicating the unmet mechanism researches for GBC. In this study, our data showed that SNHG15 expression significantly up-regulated and its high expression associated with poor overall survival of patients suffer from GBC. Functional experiments showed that SNHG15 depletion delayed the proliferation and enhanced the apoptosis of GBC tumor cells under the nutrition stress condition, which further confirmed in the subcutaneous xenograft model and liver metastasis model. Mechanistically, SNHG15 could interact with AMPK and facilitate the phosphorylation of AMPK to Tuberous sclerosis complex TSC2, resulting in mTOR suppression and autophagy enhancement, and finally, conferring the GBC cell sustain proliferation under nutrition stress. Taken together, our findings revealed that SNHG15 promotes GBC tumor progression by enhancing the autophagy under poor nutrition tumor microenvironment, which could be a promising targets for GBC.

Indexed as

CarcinomaGallbladder NeoplasmsAMP-Activated Protein KinasesAnimalsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansTumor MicroenvironmentAMP-Activated Protein KinasesautophagyGallbladder cancerSNHG15TSC2

Identifiers

PMID37937948
PMCPMC10732635
OpenAlexW4388499758

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.