Evidence map›Paper›PMID 37443143›Full record

ArticleCell death & disease2023

β-arrestin 2 negatively regulates lung cancer progression by inhibiting the TRAF6 signaling axis for NF-κB activation and autophagy induced by TLR3 and TLR4.

Ji Young Kim, Ji Hye Shin, Mi-Jeong Kim, Yeeun Kang, Ji Su Lee, Juhee Son, Soo-Kyung Jeong, Daesik Kim, Duk-Hwan Kim, Eunyoung Chun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 30 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

11 authors at 4 institutions in 1 country.

Ji Young Kim *Department of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Ji Hye Shin *Department of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Mi-Jeong KimDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Yeeun KangDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Ji Su LeeDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Juhee SonDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Soo-Kyung JeongR&D Center, CHA Vaccine Institute, Seongnam-si, 13493, Republic of Korea.
Daesik KimDepartment of Precision Medicine, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Duk-Hwan KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea.
Eunyoung ChunR&D Center, CHA Vaccine Institute, Seongnam-si, 13493, Republic of Korea. chun.eunyoung@gmail.com.
Ki-Young LeeDepartment of Immunology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, 16419, Republic of Korea. thylee@skku.edu.ORCID 0000-0002-6722-1751
Samsung (South Korea) · KRCHA Vaccine Institute (South Korea) · KRSungkyunkwan University · KRSamsung Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-arrestin 2 (ARRB2) is functionally implicated in cancer progression via various signaling pathways. However, its role in lung cancer remains unclear. To obtain clinical insight on its function in lung cancer, microarray data from lung tumor tissues (LTTs) and matched lung normal tissues (mLNTs) of primary non-small cell lung cancer (NSCLC) patients (n = 37) were utilized. ARRB2 expression levels were markedly decreased in all 37 LTTs compared to those in matched LNTs of NSCLC patients. They were significantly co-related to enrichment gene sets associated with oncogenic and cancer genes. Importantly, Gene Set Enrichment Analysis (GSEA) between three LTTs with highly down-regulated ARRB2 and three LTTs with lowly down-regulated ARRB2 revealed significant enrichments related to toll-like receptor (TLR) signaling and autophagy genes in three LTTs with highly down-regulated ARRB2, suggesting that ARRB2 was negatively involved in TLR-mediated signals for autophagy induction in lung cancer. Biochemical studies for elucidating the molecular mechanism revealed that ARRB2 interacted with TNF receptor-associated factor 6 (TRAF6) and Beclin 1 (BECN1), thereby inhibiting the ubiquitination of TRAF6-TAB2 to activate NF-κB and TRAF6-BECN1 for autophagy stimulated by TLR3 and TLR4, suggesting that ARRB2 could inhibit the TRAF6-TAB2 signaling axis for NF-κB activation and TRAF6-BECN1 signaling axis for autophagy in response to TLR3 and TLR4. Notably, ARRB2-knockout (ARRB2KO) lung cancer cells exhibited marked enhancements of cancer migration, invasion, colony formation, and proliferation in response to TLR3 and TLR4 stimulation. Altogether, our current data suggest that ARRB2 can negatively regulate lung cancer progression by inhibiting TLR3- and TLR4-induced autophagy.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAdaptor Proteins, Signal TransducingAutophagybeta-Arrestin 2HumansLungNF-kappa BTNF Receptor-Associated Factor 6Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like ReceptorsAdaptor Proteins, Signal Transducingbeta-Arrestin 2NF-kappa BTAB2 protein, humanTLR3 protein, humanTLR4 protein, humanTNF Receptor-Associated Factor 6Toll-Like Receptor 3Toll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID37443143
PMCPMC10344878
OpenAlexW4384200964

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.