Evidence map›Paper›PMID 31919718›Full record

ArticleHuman cell2020

PAK1 silencing is synthetic lethal with CDK4/6 inhibition in gastric cancer cells via regulating PDK1 expression.

Yan Qian, Xu Wu, Haixiao Wang, Guowei Hou, Xiao Han, Wei Song

Abstract read
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In one paragraph

Article in Human cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Energy metabolism: a new target for gastric cancer treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Review
  3. Review
  4. Review
  5. Article
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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.

Yan QianDepartment of Gastric, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, 223300, Jiangsu, China.
Xu WuDepartment of Gastric, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, 223300, Jiangsu, China.
Haixiao WangDepartment of Gastric, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, 223300, Jiangsu, China.
Guowei HouDepartment of Gastric, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, 223300, Jiangsu, China.
Xiao HanDepartment of Gastric, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huai'an, 223300, Jiangsu, China.
Wei SongDepartment of Gastroenterlogy, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, No. 1 Huanghe West Road, Huaiyin, Huai'an, 223300, Jiangsu, China. WeiSongdjk@163.com.ORCID http://orcid.org/0000-0003-2479-2973
Huaian First People’s Hospital · CNXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is one of the most common malignancies worldwide. The prognosis of GC is unsatisfied owning to widespread metastasis. P21-activated kinase 1 (PAK1), a member of serine/threonine kinases, is associated with the progression of multiple types of human cancers. Here, we demonstrated that CDK4/6 inhibitor reduced GC cell viability and decreased PAK1 expression. Consistently, PAK1 ablation increased GC cell sensitivity exposed to CDK4/6 inhibitor and promoted DNA damage. We also revealed PAK1 depletion notably affected PDK1-AKT pathway, and PDK1 overexpression totally abrogated the effect of PAK1 deletion on DNA damage in GC cells. Additionally, PDK1 overexpression also rescued the increased GC cell sensitivity towards CDK4/6 inhibitor and the cell cycle arrest caused by PAK1 depletion. Our findings, therefore, suggested that PAK1 silencing increased sensitivity to CDK4/6 inhibition in gastric cancer cells via PDK1-AKT pathway. We, therefore, thought PAK1 as a promising therapeutic target for the treatment of CDK4/6 inhibitor-resistant gastric cancer.

Indexed as

Gene SilencingCell Line, TumorCyclin-Dependent Kinase 4Gene Expression Regulation, NeoplasticHumansp21-Activated KinasesStomach NeoplasmsCDK4 protein, humanCyclin-Dependent Kinase 4p21-Activated KinasesPAK1 protein, humanCDK4/6 inhibitorGastric cancer (GC)P21-activated kinase 1 (PAK1)PDK1 pathwayProliferation

Identifiers

PMID31919718
OpenAlexW3000281791

What OpenQuestion holds

Textmetadata
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.