Evidence map›Paper›PMID 30944308›Full record

ArticleCell death & disease2019

VPS33B interacts with NESG1 to modulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling and induce 5-fluorouracil sensitivity in nasopharyngeal carcinoma.

Zixi Liang, Zhen Liu, Chao Cheng, Hao Wang, Xiaojie Deng, Jiahao Liu, Chen Liu, Yonghao Li, Weiyi Fang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 71 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 4 institutions in 1 country.

Zixi LiangCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Zhen LiuCancer Center, School of Basic Medical Science, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Chao ChengCancer Center, School of Basic Medical Science, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Hao WangCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Xiaojie DengCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Jiahao LiuCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Chen LiuCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Yonghao LiCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China.
Weiyi FangCancer Center, Integrated Hospital of Traditional Chinese Medicine, Southern Medical University, 510310, Guangzhou, Guangdong, P. R. China. fangweiyi1975@163.com.
TCM-Intigrated Cancer Center of Southern Medical University · CNSouthern Medical University · CNGuangzhou Medical University · CNSouthern Medical University Shenzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The vacuolar protein sorting 33B (VPS33B) was rarely reported in malignant tumors. In this research, we demonstrated that overexpression of VPS33B inhibited proliferation and chemoresistance to fluorouracil (5-FU) in nasopharyngeal carcinoma (NPC) in vivo and in vitro. Mechanistic analysis confirmed that overexpression of VPS33B modulated EGFR/PI3K/AKT/c-Myc/P53 signaling to arrest the cell cycle at G1/S phase. In addition, miR-133a-3p, a tumor-suppressive miRNA, was induced by P53 and directly targeted the EGFR/PI3K/AKT/c-Myc/P53 signaling and thus formed a negative feedback loop. Furthermore, another tumor suppressor, NESG1, interacted with VPS33B by colocalizing in the cytoplasm. The knockdown of NESG1 reversed the inhibitory effects of the overexpression of VPS33B in NPC cells by downregulating the PI3K/AKT/c-Jun-mediated transcription repression. Surprisingly, VPS33B was downregulated in the nicotine-treated and LMP-1-overexpressing NPC cells by targeting PI3K/AKT/c-Jun-mediated signaling. In addition, patients with higher VPS33B expression had a longer overall survival. Our study is the first to demonstrate that VPS33B is negatively regulated by LMP-1 and nicotine and thus suppresses the proliferation of NPC cells by interacting with NESG1 to regulate EGFR/PI3K/AKT/c-Myc/P53/miR-133a-3p signaling in NPC cells.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntimetabolites, AntineoplasticCell Line, TumorCell ProliferationCytoskeletal ProteinsErbB ReceptorsFemaleFluorouracilGene Expression Regulation, NeoplasticHumansLIM Domain ProteinsMaleMiceMice, Inbred BALB CMice, NudeAdaptor Proteins, Signal TransducingAntimetabolites, AntineoplasticCFAP45 protein, humanCytoskeletal ProteinsEGFR protein, humanErbB ReceptorsFluorouracilLIM Domain ProteinsMicroRNAsMIRN133 microRNA, humanPDLIM7 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycTumor Suppressor Protein p53Vesicular Transport ProteinsVPS33B protein, human

Identifiers

PMID30944308
PMCPMC6447525
OpenAlexW2928763532

What OpenQuestion holds

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LicenceCC BY
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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.