Evidence map›Paper›PMID 33683834›Full record

ArticleFEBS open bio2021

The lncRNA ALMS1-IT1 may promote malignant progression of lung adenocarcinoma via AVL9-mediated activation of the cyclin-dependent kinase pathway.

Tian Luan, Tian-Ye Zhang, Zhong-Hua Lv, Bi-Xi Guan, Jian-Yu Xu, Jian Li, Ming-Xu Li, Song-Liu Hu

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Review
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  16. Cross-Talk Between mFrontiers in immunology · 2022
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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 1 institution in 1 country.

Tian LuanDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Tian-Ye ZhangDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Zhong-Hua LvDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Bi-Xi GuanDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Jian-Yu XuDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Jian LiDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Ming-Xu LiDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Song-Liu HuDepartment of Radiation Oncology, Harbin Medical University Cancer Hospital, Harbin, China.ORCID 0000-0003-2924-1222
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is the primary epithelial tumor of the lung. The lack of clinical symptoms and specific molecular diagnostic indicators during the early stages of LUAD mean that the disease may not be detected until late stages, and the 5-year survival rate is only approximately 15%. Long non-coding RNA ALMS1 intronic script 1 (ALMS1-IT1) was previously reported to be correlated with the poor prognosis of head and neck squamous cell carcinoma patients. Here, we investigated whether ALMS1-IT1 has prognostic potential for LUAD. Bioinformatics analyses were performed to examine the expression and prognostic value of ALMS1 and AVL9 (for which gene expression is positively correlated with ALMS1-IT1 expression in LUAD) in LUAD based on TCGA and Oncomine databases. We report that ALMS1-IT1 and AVL9 were both highly expressed in LUAD and correlated with poor outcomes in LUAD patients. Of note, the prognosis of LUAD patients with low expression of both ALMS1-IT1 and AVL9 was superior to that of other patients. Furthermore, the proliferation, migration and invasion of LUAD cells were decreased in cells lacking ALMS1-IT1, and this decrease could be almost completely reversed through overexpression of AVL9. Gene set enrichment analysis revealed that expression of genes related to the cell cycle pathway is closely related to both the high expression of ALMS1-IT1 and AVL9 in LUAD. Finally, up-regulation of ALMS1-IT1 can activate the cyclin-dependent kinase pathway, whereas absence of AVL9 can reverse this activation, as shown by western blotting. In summary, ALMS1-IT1/AVL9 may promote the malignant progression of LUAD, at least in part by regulating the cyclin-dependent kinase pathway.

Indexed as

AdenocarcinomaAdenocarcinoma of LungCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationChinaCyclin-Dependent KinasesDatabases, GeneticHumansIntronsLungLung NeoplasmsPrognosisRNA InterferenceRNA, Long NoncodingALMS1 protein, humanAVL9 protein, humanCell Cycle ProteinsCyclin-Dependent KinasesRNA, Long NoncodingVesicular Transport ProteinsALMS1-IT1AVL9CDK pathwaylung adenocarcinomaprognosis

Identifiers

PMID33683834
PMCPMC8091588
OpenAlexW3134702276

What OpenQuestion holds

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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 OpenQuestion graph.