Evidence map›Paper›PMID 34337857›Full record

ArticleThe Kaohsiung journal of medical sciences2021

LncRNA CASC2 inhibits lung adenocarcinoma progression through forming feedback loop with miR-21/p53 axis.

Zhi-Hui Wu, Juan Zhou, Guo-Hong Hu, Jie Liu, Wen-Can Li, Xi-Hua Lai, Min Liu

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2021. 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
1.0field-weighted citation impact, top 29% 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, 14 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Zhi-Hui WuDepartment of Thoracic Surgery, Zhuzhou Central Hospital, Zhuzhou, People's Republic of China.
Juan ZhouDepartment of Pulmonary and Critical Care Medicine, Zhuzhou Central Hospital, Zhuzhou, People's Republic of China.
Guo-Hong HuDepartment of Pediatrics, Zhuzhou Central Hospital, Zhuzhou, People's Republic of China.
Jie LiuDepartment of Basic Medicine, Hunan Traditional Chinese Medical College, Zhuzhou, People's Republic of China.
Wen-Can LiDepartment of Thoracic Surgery, Zhuzhou Central Hospital, Zhuzhou, People's Republic of China.
Xi-Hua LaiDepartment of Thoracic Surgery, Zhuzhou Central Hospital, Zhuzhou, People's Republic of China.
Min LiuDepartment of Oncology, Zhuzhou Central Hospital, Zhuzhou, People's Republic of China.ORCID https://orcid.org/0000-0002-3106-6059
Zhuzhou Central Hospital · CNHunan Academy of Traditional Chinese Medicine · CN

Funding

Natural Science Foundation of Hunan Province 2018JJ4094
6 · The paper itself

Abstract

Lung adenocarcinoma (LUAD) is the most common type of lung cancer. Currently, the survival rate of LUAD patients remains low due to heterogeneity and high invasiveness. The long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is reported to be related to LUAD development. Hence, we investigate the roles and regulatory mechanism of CASC2 in LUAD. The expression levels of CASC2, microRNA (miR)-21, and p53 were quantified by quantitative real-time polymerase chain reaction, and the protein levels of Bax, Bcl-2, p53, and p21 were examined using western blotting. A dual-luciferase reporter experiment was conducted to prove the molecular interactions between CASC2 and miR-21 or p53. CCK-8 and flow cytometry assays were conducted to assess cell proliferation and apoptosis, respectively. CASC2 was expressed at a low level in LUAD patients and LUAD cell lines. CASC2 overexpression markedly suppressed cell proliferation and enhanced apoptosis. Mechanistically, CASC2 overexpression dramatically inhibited miR-21 expression and increased p53 expression by directly targeting miR-21. Moreover, rescue experiments suggested that either miR-21 overexpression or p53 silencing obviously weakened the biological effects of CASC2 overexpression. In addition, p53 was proven to be an upstream transcription factor of CASC2 and can activate CASC2 transcription. These results provide evidence that the lncRNA CASC2/miR-21/p53 form a positive feedback loop to mediate cell proliferation and apoptosis in LUAD, which may provide a new insight into the pathological mechanisms of LUAD.

Indexed as

Adenocarcinoma of LungDisease ProgressionHumansLung NeoplasmsMicroRNAsTumor Suppressor Protein p53Tumor Suppressor Proteinslong non-coding RNA CASC2, humanMicroRNAsMIRN21 microRNA, humanTP53 protein, humanTumor Suppressor Protein p53Tumor Suppressor ProteinsapoptosislncRNA CASC2lung adenocarcinomamiR-21proliferation

Identifiers

PMID34337857
PMCPMC11896527
OpenAlexW3190649843

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.