Evidence map›Paper›PMID 31632968›Full record

ArticleFrontiers in cell and developmental biology2019

Novel Function of lncRNA ADAMTS9-AS2 in Promoting Temozolomide Resistance in Glioblastoma via Upregulating the FUS/MDM2 Ubiquitination Axis.

Yuanliang Yan, Zhijie Xu, Xi Chen, Xiang Wang, Shuangshuang Zeng, Zijin Zhao, Long Qian, Zhi Li, Jie Wei, Lei Huo and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cell and developmental biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.9field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 97 citations in OpenAlex.

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9 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Yuanliang YanDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Zhijie XuDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, China.
Xi ChenDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Xiang WangDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Shuangshuang ZengDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Zijin ZhaoDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.
Long QianDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Zhi LiKey Laboratory for Molecular Radiation Oncology of Hunan Province, Center for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Jie WeiDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Lei HuoDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.
Xuejun LiDepartment of Neurosurgery, Xiangya Hospital, Central South University, Changsha, China.
Zhicheng GongDepartment of Pharmacy, Xiangya Hospital, Central South University, Changsha, China.
Lunquan SunKey Laboratory for Molecular Radiation Oncology of Hunan Province, Center for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, China.
Xiangya Hospital Central South University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLncRNAs have been shown to play essential roles in cancer therapeutic response. However, the detailed mechanism of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remain to be elucidated.

methodsTo elucidate the mechanism maintaining TMZ resistance, we constructed two TMZ-resistant GBM cell lines (T98G-R/U118-R). LncRNAs from four public datasets were reanalyzed, and the candidate lncRNA ADAMTS9-AS2 was evaluated in TMZ-treated GBM patients and

resultsReanalysis of lncRNA expression profiles identified ADAMTS9-AS2 as significantly overexpressed in TMZ-resistant GBM cells and as positively associated with the IC

conclusionADAMTS9-AS2 possessed a novel function that promotes TMZ resistance via upregulating the FUS/MDM2 axis in GBM cells. The RRM or Znf_RanBP2 domains of FUS facilitate the combination of ADAMTS9-AS2 and FUS, competitively inhibiting MDM2-dependent FUS K48 ubiquitination and resulting in enhanced FUS stability and TMZ resistance. Our results suggest that the ADAMTS9-AS2/FUS/MDM2 axis may represent a suitable prognostic biomarker and a potential target in TMZ-resistant GBM therapy.

Indexed as

ADAMTS9-AS2FUSglioblastomaMDM2TMZ resistanceubiquitination

Identifiers

PMID31632968
PMCPMC6783494
OpenAlexW2979114017

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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.