Evidence map›Paper›PMID 37884580›Full record

ArticleCancer gene therapy2023

LncRNA CALML3-AS1 modulated by m

Heng Zhang, Shao-Qiang Wang, Jie-Bo Zhu, Li-Na Wang, Hang Lin, Lin-Feng Li, Yuan-Da Cheng, Chao-Jun Duan, Chun-Fang Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. The mCells · 2026
    Review
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  7. Cis-Regulation of an mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

9 authors at 3 institutions in 2 countries.

Heng ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China. 404346@csu.edu.cn.ORCID 0000-0002-1554-2051
Shao-Qiang WangDepartment of Thoracic Surgery, Weifang People's Hospital, Weifang Medical University, Weifang, 261041, Shandong Province, P.R. China.
Jie-Bo ZhuDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
Li-Na WangDepartment of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Jining, 272029, Shandong Province, P. R. China.
Hang LinDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
Lin-Feng LiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
Yuan-Da ChengDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
Chao-Jun DuanDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China.
Chun-Fang ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, P. R. China. zhcf3801@csu.edu.cn.
Central South University · CNAffiliated Hospital of Jining Medical University · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is a common and lethal malignancy. The carcinogenic roles of lncRNA CALML3 antisense RNA 1 (CALML3-AS1) have been documented. However, the function and potential mechanisms of CALML3-AS1 in the progression of NSCLC need to be further explored. The molecule expression was assessed by qRT-PCR and Western blot. The subcellular localization of CALML3-AS1 was observed by fluorescence in situ hybridization (FISH). The malignant behaviors of NSCLC cells were evaluated by CCK-8, colony formation, EdU, wound healing and transwell assays. In vivo xenograft tumor and liver metastatic models were established. The molecular mechanisms were investigated by RIP, RNA pull-down and ChIP assays. The methylation level was detected by MSP. Herein, we found that CALML3-AS1 was upregulated, while butyrophilin-like 9 (BTNL9) was downregulated in NSCLC. Functionally, CALML3-AS1 depletion repressed NSCLC cell malignant phenotypes, in vivo tumor growth, and liver metastasis. Mechanistically, AlkB homolog 5 (ALKBH5) enhanced CALML3-AS1 stability via N

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, Long NoncodingRNA MethylationButyrophilinsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansIn Situ Hybridization, FluorescenceMethylationBTNL9 protein, humanButyrophilinsMicroRNAsRNA, Long Noncoding

Identifiers

PMID37884580
OpenAlexW4387952864

What OpenQuestion holds

Textmetadata
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.