Evidence map›Paper›PMID 31557618›Full record

ArticleMolecular therapy. Nucleic acids2019

Long Non-coding RNA LINC00628 Interacts Epigenetically with the LAMA3 Promoter and Contributes to Lung Adenocarcinoma.

Shu-Feng Xu, Yue Zheng, Ling Zhang, Ping Wang, Chun-Mi Niu, Tong Wu, Qi Tian, Xiao-Bo Yin, Shan-Shan Shi, Lei Zheng and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 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

11 authors at 4 institutions in 1 country.

Shu-Feng XuDepartment of Respiratory, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China.
Yue ZhengDepartment of Oncology, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China.
Ling ZhangDepartment of Respiratory, Hebei Chest Hospital, Shijiazhuang 050021, P.R. China.
Ping WangDepartment of Respiratory, Chinese PLA General Hospital, Beijing 100853, P.R. China.
Chun-Mi NiuDepartment of Respiratory, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China.
Tong WuMedical Students, Hebei Medical University, Shijiazhuang 050017, P.R. China.
Qi TianDepartment of Respiratory, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China.
Xiao-Bo YinDepartment of Respiratory, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China.
Shan-Shan ShiMedical Students, Hebei Medical University, Shijiazhuang 050017, P.R. China.
Lei ZhengDepartment of Oncology, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China.
Li-Ming GaoDepartment of Oncology, The First Hospital of Qinhuangdao, Qinhuangdao 066000, P.R. China. Electronic address: Tshgaoliming@sina.com.
First Hospital of Qinhuangdao · CNHebei Medical University · CNChinese PLA General Hospital · CNHospital of Hebei Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNAs (lncRNAs) have emerged as key regulators of cellular progress in lung adenocarcinoma. In this study, to identify cancer-related lncRNAs and genes, we screened for those lncRNAs that were differentially expressed in lung adenocarcinoma, which revealed LINC00628 overexpression and low expression of laminin subunit alpha 3 (LAMA3). This was further validated in the cancerous tissues from patients diagnosed with lung adenocarcinoma. Thereafter, we explored the functional relevance of LINC00628 and LAMA3 in lung adenocarcinoma by analyzing the recruitment of DNA methyltransferase (DNMT) and the cellular processes of lung adenocarcinoma cells following treatments that induced LINC00628 overexpression or LINC00628 silencing or with 5-azacytidine (5-Aza, a DNMT inhibitor). The results showed that LINC00628 silencing decreased cell proliferation, migration, and invasion as well as the drug resistance of lung adenocarcinoma cells to vincristine (VCR). The results were opposite in the cells with LAMA3 demethylation induced by 5-Aza treatment. Further research indicated that LINC00628 recruited DNMT1, DNMT3A, and DNMT3B to promote the methylation of LAMA3 promoter, thereby decreasing its expression. Moreover, an in vivo experiment was performed in nude mice to assess the tumor growth ability and drug resistance of human lung adenocarcinoma cells. It was observed that LINC00628 silencing or 5-Aza treatment inhibited the in vivo tumor growth ability of the human lung adenocarcinoma cells and reduced their resistance to VCR. Altogether, our results provide evidence of a mechanism by which LINC00628 silencing exerts an inhibitory role in lung adenocarcinoma by modulating the DNA methylation of LAMA3, indicative of a novel molecular target for treatment of lung adenocarcinoma patients showing resistance to VCR.

Indexed as

drug resistanceinvasionLAMA3long non-coding RNA LINC00628lung adenocarcinomamethylationmigrationvincristine

Identifiers

PMID31557618
PMCPMC6796683
OpenAlexW2967875992

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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.