Evidence map›Paper›PMID 29805560›Full record

ArticleOncology letters2018

Evaluation of the prognostic and physiological functions of death associated protein kinase 1 in breast cancer.

Yide Huang, Meizhen Lin, Xiangjin Chen, Chaoqun Huang, Xiuli Zhang, Ling Chen, Kunlin Wu, Yupeng Chen, Youzhi Zhu, Yao Lin

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. 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

10 authors at 3 institutions in 1 country.

Yide HuangProvincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou, Fujian 350117, P.R. China.
Meizhen LinProvincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou, Fujian 350117, P.R. China.
Xiangjin ChenDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350000, P.R. China.
Chaoqun HuangProvincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou, Fujian 350117, P.R. China.
Xiuli ZhangProvincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou, Fujian 350117, P.R. China.
Ling ChenDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350000, P.R. China.
Kunlin WuDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350000, P.R. China.
Yupeng ChenDepartment of Pathology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350000, P.R. China.
Youzhi ZhuDepartment of Thyroid and Breast Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350000, P.R. China.
Yao LinProvincial University Key Laboratory of Cellular Stress Response and Metabolic Regulation, College of Life Sciences, Fujian Normal University, Fuzhou, Fujian 350117, P.R. China.
Fujian Normal University · CNFujian Medical University · CNFirst Affiliated Hospital of Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Death associated protein kinase 1 (DAPK1) is a notable serine/threonine kinase involved in the regulation of multiple cellular pathways, including apoptosis and autophagy. Although DAPK1 is usually considered to be a tumor suppressor, it was previously reported to promote the viability of p53 mutant cancer cell lines and possess physiological oncogenic functions in breast cancer. However, the ability of endogenous DAPK1 to suppress breast cancer cell mobility has not been assessed. In the present study, the prognostic function of DAPK1 in a Chinese patient cohort was evaluated, and no significant association was observed between DAPK1 expression and patient survival or lymph node metastasis. In order to investigate the physiological function of endogenous DAPK1, stable inducible DAPK1 knockdown MCF7 and MDA-MB-231 cell lines were established. Consistent with previous studies, endogenous DAPK1 only regulated cell viability in p53 mutant MDA-MB-231 cells. However, knockdown of DAPK1 did not significantly affect cell motility of either MCF7 or MDA-MB-231 cells. Altogether, these results further explored the function of endogenous DAPK1 in breast cancer and may shed light in understanding the molecular signaling pathways regulating the physiological function of DAPK1.

Indexed as

breast cancerdeath associated protein kinase 1invasionmigrationproliferation

Identifiers

PMID29805560
PMCPMC5958705
OpenAlexW2795540299

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.