Evidence map›Paper›PMID 38970088›Full record

ArticleRespiratory research2024

CALU promotes lung adenocarcinoma progression by enhancing cell proliferation, migration and invasion.

Yan Li, Shengnan Sun, Hui Zhang, Yongjian Jing, Xingzhao Ji, Qiang Wan, Yi Liu

Abstract read
In one paragraph

Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

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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.

Yan Li *Department of Pulmonary and Critical Care Medicine, The Second Hospital of Shandong University, Jinan, Shandong, 250033, China.
Shengnan Sun *Key Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Hui ZhangDepartment of Pulmonary and Critical Care Medicine, Shandong Provincial Hospital, Shandong University, Jinan, Shandong, 250021, China.
Yongjian JingThe First People's Hospital of Pingyuan County, Dezhou, Shandong, 253100, China.
Xingzhao JiKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Qiang WanKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China. wanqiang@sdu.edu.cn.
Yi LiuKey Laboratory of Cell Metabolism in Medical and Health of Shandong Provincial Health Commission, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China. liuyishanyi@email.sdu.edu.cn.

Funding

the National Natural Science Foundation of China 82070756the National Natural Science Foundation of China 82071569the National Natural Science Foundation of China 82200049the Shandong Provincial Natural Science Foundation ZR2023QH316
6 · The paper itself

Abstract

backgroundLung cancer is the second most common cancer with the highest mortality in the world. Calumenin as a molecular chaperone that not only binds various proteins within the endoplasmic reticulum but also plays crucial roles in diverse processes associated with tumor development. However, the regulatory mechanism of calumenin in lung adenocarcinoma remains elusive. Here, we studied the impact of calumenin on lung adenocarcinoma and explored possible mechanisms.

methods5-ethynyl-2'-deoxyuridine assay, colony formation, transwell and wound healing assays were performed to explore the effects of calumenin on the proliferation and migration of lung adenocarcinoma cells. To gain insights into the underlying mechanisms through which calumenin knockdown inhibits the migration and proliferation of lung adenocarcinoma, we performed Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis and Ingenuity Pathway Analysis based on transcriptomics by comparing calumenin knockdown with normal A549 cells.

resultsThe mRNA and protein levels of calumenin in lung adenocarcinoma are highly expressed and they are related to an unfavorable prognosis in this disease. Calumenin enhances the proliferation and migration of A549 and H1299 cells. Gene Set Enrichment Analysis revealed that knockdown of calumenin in A549 cells significantly inhibited MYC and V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog signaling pathways while activating interferon signals, inflammatory signals, and p53 pathways. Ingenuity pathway analysis provided additional insights, indicating that the interferon and inflammatory pathways were prominently activated upon calumenin knockdown in A549 cells.

conclusionsThe anti-cancer mechanism of calumenin knockdown might be related to the inhibition of MYC and KRAS signals but the activation of interferon signals, inflammatory signals and p53 pathways.

Indexed as

Adenocarcinoma of LungCell MovementCell ProliferationLung NeoplasmsNeoplasm InvasivenessA549 CellsCalcium-Binding ProteinsDisease ProgressionGene Expression Regulation, NeoplasticHumansCalcium-Binding ProteinsCalumeninIngenuity pathway analysisLung adenocarcinomaMigrationProliferation

Identifiers

PMID38970088
PMCPMC11227236

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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.