Evidence map›Paper›PMID 38341418›Full record

ArticleCell death discovery2024

Hsa_circ_0021205 enhances lipolysis via regulating miR-195-5p/HSL axis and drives malignant progression of glioblastoma.

Suwen Li, Jiaqi Yuan, Zhe Cheng, Yongdong Li, Shan Cheng, Xinglei Liu, Shilu Huang, Zhipeng Xu, Anyi Wu, Liang Liu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
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

11 authors at 2 institutions in 1 country.

Suwen Li *Department of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID http://orcid.org/0000-0001-7567-071X
Jiaqi Yuan *Department of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Zhe Cheng *Department of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Yongdong LiDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Shan ChengDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Xinglei LiuDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Shilu HuangDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Zhipeng XuDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Anyi WuDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China.
Liang LiuDepartment of Neurosurgery, Affiliated Nanjing Brain Hospital, Nanjing Medical University, Nanjing, Jiangsu, China.
Jun DongDepartment of Neurosurgery, the Second Affiliated Hospital of Soochow University, Suzhou, China. dongjun@suda.edu.cn.ORCID http://orcid.org/0000-0002-0026-6680
Soochow University · CNNanjing Brain Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal lipid metabolism is an essential hallmark of glioblastoma. Hormone sensitive lipase (HSL), an important rate-limiting enzyme contributed to lipolysis, which was involved in aberrant lipolysis of glioblastoma, however, its definite roles and the relevant regulatory pathway have not been fully elucidated. Our investigations disclosed high expression of HSL in glioblastoma. Knock-down of HSL restrained proliferation, migration, and invasion of glioblastoma cells while adding to FAs could significantly rescue the inhibitory effect of si-HSL on tumor cells. Overexpression of HSL further promoted tumor cell proliferation and invasion. Bioinformatics analysis and dual-luciferase reporter assay were performed to predict and verify the regulatory role of ncRNAs on HSL. Mechanistically, hsa_circ_0021205 regulated HSL expression by sponging miR-195-5p, which further promoted lipolysis and drove the malignant progression of glioblastoma. Besides, hsa_circ_0021205/miR-195-5p/HSL axis activated the epithelial-mesenchymal transition (EMT) signaling pathway. These findings suggested that hsa_circ_0021205 promoted tumorigenesis of glioblastoma through regulation of HSL, and targeting hsa_circ_0021205/miR-195-5p/HSL axis can serve as a promising new strategy against glioblastoma.

Identifiers

PMID38341418
PMCPMC10858904
OpenAlexW4391721787

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.