Evidence map›Paper›PMID 36418890›Full record

ArticleCell death & disease2022

BTN3A1 promotes tumor progression and radiation resistance in esophageal squamous cell carcinoma by regulating ULK1-mediated autophagy.

Wenjing Yang, Bo Cheng, Pengxiang Chen, Xiaozheng Sun, Zhihua Wen, Yufeng Cheng

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  16. The role of autophagy in hypoxia-induced radioresistance.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2023
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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

6 authors at 2 institutions in 1 country.

Wenjing YangDepartment of Radiation Oncology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.ORCID 0000-0001-8451-8189
Bo ChengDepartment of Radiation Oncology, Shandong Cancer Hospital and Institute, Cheeloo College of Medicine, Shandong University, 250012, Jinan, Shandong, P. R. China.
Pengxiang ChenDepartment of Radiation Oncology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Xiaozheng SunDepartment of Radiation Oncology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Zhihua Wen *Department of Radiation Oncology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China. wenzhihua1101@126.com.ORCID 0000-0003-4755-1136
Yufeng Cheng *Department of Radiation Oncology, Qilu Hospital of Shandong University, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China. qlcyf@sdu.edu.cn.ORCID 0000-0003-1466-3115
Qilu Hospital of Shandong University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy is one of the most effective treatments for esophageal squamous cell carcinoma (ESCC); however, radioresistance is a clinical problem that must urgently be solved. Here, we found that butyrophilin subfamily 3 member A1 (BTN3A1) is upregulated in ESCC tumor tissues compared with nontumor tissues. We also evaluated BTN3A1 expression in patients with ESCC receiving adjuvant radiotherapy. The results demonstrated that BTN3A1 upregulation predicts a poor prognosis for ESCC patients. BTN3A1 overexpression promotes ESCC cell proliferation in vitro and in vivo. Moreover, BTN3A1 knockdown sensitized ESCC cells to radiation. We further explored the mode of death involved in BTN3A1-mediated radioresistance. Previous studies have shown that apoptosis, autophagy, necrosis, pyroptosis and ferroptosis are important for the survival of ESCC cells. We performed an RT-PCR array and western blotting (WB) to identify the mode of death and revealed for the first time that BTN3A1 promotes cell radioresistance by activating autophagy. In addition, by performing immunoprecipitation and mass spectrometry analyses, we found that BTN3A1 regulated the expression of UNC-51-like autophagy activating kinase 1(ULK1) and promoted its phosphorylation to subsequently initiate autophagy. Chromatin immunoprecipitation (ChIP) and luciferase reporter assay results indicated that BTN3A1 is a novel direct target of hypoxia inducible factor-1α (HIF-1α). HIF-1α, a transcription factor, promotes BTN3A1 transcription upon irradiation. Overall, the present study is the first to show that BTN3A1 plays a key role in radioresistance and that targeting BTN3A1 might be a promising strategy to improve radiotherapy efficacy in patients with ESCC.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaAntigens, CDApoptosisAutophagyAutophagy-Related Protein-1 HomologButyrophilinsCell Line, TumorHumansIntracellular Signaling Peptides and ProteinsAntigens, CDAutophagy-Related Protein-1 HomologBTN3A1 protein, humanButyrophilinsIntracellular Signaling Peptides and ProteinsULK1 protein, human

Identifiers

PMID36418890
PMCPMC9684582
OpenAlexW4309715129

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.