Evidence map›Paper›PMID 33021072›Full record

ArticleJournal of cellular and molecular medicine2020

DEPDC1 up-regulates RAS expression to inhibit autophagy in lung adenocarcinoma cells.

Wei Wang, Aili Li, Xiaodan Han, Qingqing Wang, Jinyong Guo, Youru Wu, Chen Wang, Guojin Huang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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  14. [DEPDC1 is Highly Expressed in Lung Adenocarcinoma and Promotes Tumor Cell Proliferation].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2021
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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

8 authors at 1 institution in 1 country.

Wei WangLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Aili LiLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Xiaodan HanLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Qingqing WangLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Jinyong GuoLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Youru WuLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Chen WangLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.
Guojin HuangLaboratory of Respiratory Diseases, the Affiliated Hospital of Guilin Medical University, Guilin, China.ORCID 0000-0001-7020-5528
Guilin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DEP domain containing 1(DEPDC1) is involved in the tumorigenesis of a variety of cancers. But its role in tumorigenesis of lung adenocarcinoma (LUAD) is not fully understood. Here, we investigated the role and the underlying mechanisms of DEPDC1 in the development of LUAD. The expression and prognostic values of DEPDC1 in LUAD were analysed by using the data from public databases. Gene enrichment in TCGA LUAD was analysed using GSEA software with the pre-defined gene sets. Cell proliferation, migration and invasion of A549 cells were examined with colony formation, Transwell and wound healing assays. The function of DEPDC1 in autophagy and RAS-ERK1/2 signalling was determined with Western blot assay upon DEPDC1 knockdown and/or overexpression in A549, HCC827 and H1993 cells. The results demonstrated that DEPDC1 expression was up-regulated in LUAD tissues, and its high expression was correlated with unfavourable prognosis. The data also showed that DEPDC1 knockdown impaired proliferation, migration and invasion of A549 cells. Most notably, the results showed that DEPDC1 up-regulated RAS expression and thus enhanced ERK1/2 activity, through which DEPDC1 could inhibit autophagy. In conclusion, our study revealed that DEPDC1 is up-regulated in LUAD tissues and plays an oncogenic role in LUAD, and that DEPDC1 inhibits autophagy through the RAS-ERK1/2 signalling in A549, HCC827 and H1993 cells.

Indexed as

AutophagyA549 CellsAdenocarcinomaCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGTPase-Activating ProteinsHumansKaplan-Meier EstimateLung NeoplasmsNeoplasm ProteinsPhosphorylationPrognosisras ProteinsSignal TransductionDEPDC1 protein, humanGTPase-Activating ProteinsNeoplasm Proteinsras ProteinsA549 cellsautophagyDEPDC1H1993 cellsHCC827 cellslung adenocarcinomaRAS

Identifiers

PMID33021072
PMCPMC7701574
OpenAlexW3090587243

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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.