Evidence map›Paper›PMID 34422995›Full record

ArticleAnnals of translational medicine2021

DAPK2 activates NF-κB through autophagy-dependent degradation of I-κBα during thyroid cancer development and progression.

Yan Jiang, Ji Liu, Hua Xu, Xiao Zhou, Liu He, Chenfang Zhu

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. 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
2.9field-weighted citation impact, top 9% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Non-Apoptotic Programmed Cell Death in Thyroid Diseases.Pharmaceuticals (Basel, Switzerland) · 2022
    Review
  8. Article
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 4 institutions in 1 country.

Yan JiangDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Ji LiuDepartment of Anesthesia, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Hua XuDepartment of General Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Discipline Construction Research Center of China Hospital Development Institute, Shanghai Jiao Tong University, Shanghai, China.
Xiao ZhouDepartment of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Liu HeDepartment of General Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Discipline Construction Research Center of China Hospital Development Institute, Shanghai Jiao Tong University, Shanghai, China.
Chenfang ZhuDepartment of General Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Discipline Construction Research Center of China Hospital Development Institute, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Ninth People's Hospital · CNShanghai Pulmonary Hospital · CNShanghai Jiao Tong University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDeath-associated protein kinase 2 (DAPK2) is a serine/threonine kinase, which has been implicated in autophagy and apoptosis. DAPK2 functions as a tumor suppressor in various cancers. However, the role of DAPK2 in thyroid cancer (TC) is unclear.

methodsRNA sequencing of human TC samples was performed to identify differentially expressed genes that may play a role in TC development. The messenger RNA (mRNA) expression of DAPK2 was verified by quantitative real-time polymerase chain reaction (qRT-PCR). To investigate the role of DAPK2 in TC development, DAPK2 was knocked down and overexpressed in a TTA1 cell line. The effect of DAPK2 on cell proliferation, sensitization of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis and tumor growth was examined. The effect of DAPK2 on autophagy and NF-κB activation was investigated to address the underlying mechanism.

resultsDAPK2 was upregulated in TC. Knockdown of DAPK2 in TTA1 cells led to reduced cell proliferation, sensitization of TRAIL-induced apoptosis, and restricted tumor growth both

conclusionsOur findings revealed a pivotal role of DAPK2 in thyroid carcinogenesis, being required for tumor growth and for resistance to TRAIL-induced apoptosis through autophagy-mediated I-κBα degradation. This result provides a novel target for the therapy of TC.

Indexed as

autophagyDeath-associated protein kinase 2 (DAPK2)I-κBαnuclear factor-κB (NF-κB)thyroid cancer (TC)

Identifiers

PMID34422995
PMCPMC8339828
OpenAlexW3169761362

What OpenQuestion holds

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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.