Evidence map›Paper›PMID 34140780›Full record

ArticleOncoTargets and therapy2021

G9a Regulates Cell Sensitivity to Radiotherapy via Histone H3 Lysine 9 Trimethylation and CCDC8 in Lung Cancer.

Yunfen Li, Zhengting Chen, Ke Cao, Lan Zhang, Yuhui Ma, Shuhui Yu, Hanyu Jin, Xiaoling Liu, Wenhui Li

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 11 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

9 authors at 1 institution in 1 country.

Yunfen Li *Department of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Zhengting Chen *Department of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.ORCID 0000-0001-7461-2796
Ke Cao *Department of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Lan Zhang *Department of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Yuhui MaDepartment of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Shuhui YuDepartment of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Hanyu JinDepartment of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Xiaoling LiuDepartment of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.
Wenhui LiDepartment of Radiotherapy, Third Affiliated Hospital of Kunming Medical, Yunnan Cancer Hospital, Kunming City, Yunnan Province, People's Republic of China.ORCID 0000-0003-3019-0450
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo investigate the role and underlying mechanism of G9a and CCDC8 in lung cancer radioresistance.

methodsWestern blotting assays were used for G9a, CCDC8, H3K9me3 expression detection. MTT assays and clone formation assays were used for measuring cell proliferation activities. Flow cytometry assays were used for cell apoptosis detection. The enrichment of H3K9me3 in CCDC8 promoter was measured by chromatin immunoprecipitation assay.

resultsG9a and G9a-mediated H3K9me3 are upregulated in radioresistant lung cancer cells (A549/IR cell and XWLC-05/IR cell). Blocking G9a not only promotes radiosensitivity of A549/IR cell and XWLC-05/IR cell but also reduces aggressive behavior of radioresistant A549 cell/IR and XWLC-05/IR cell. In addition, G9a-controlled H3K9me3 is able to binding to the promoter of tumor suppressor gene CCDC8 and suppresses CCDC8 expression. CCDC8 dysregulation is responsible for G9a-mediated radioresistance of A549/IR cell and XWLC-05/IR cell.

conclusionG9a and H3K9me3 contribute to the lung cancer radioresistance via modulating CCDC8 expression.

Indexed as

CCDC8G9aH3K9me3lung cancerradiotherapy

Identifiers

PMID34140780
PMCPMC8203200
OpenAlexW3166020354

What OpenQuestion holds

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LicenceCC BY-NC
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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.