Evidence map›Paper›PMID 31713447›Full record

ArticleCell cycle (Georgetown, Tex.)2019

Co-targeting CK2α and YBX1 suppresses tumor progression by coordinated inhibition of the PI3K/AKT signaling pathway.

Wen-Fei Xu, Yi-Cong Ma, Hou-Shi Ma, Long Shi, Hang Mu, Wen-Bin Ou, Jie Peng, Ting-Ting Li, Tianyi Qin, Hai-Meng Zhou and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. 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
0.3field-weighted citation impact, top 40% 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, 10 citations in OpenAlex.

  1. Review
  2. YB1 and its role in osteosarcoma: a review.Frontiers in oncology · 2024
    Review
  3. Article
  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

12 authors at 6 institutions in 2 countries.

Wen-Fei XuCollege of Life Sciences, Jilin University, Changchun, China.
Yi-Cong MaZhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Zhejiang, China.
Hou-Shi MaZhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Zhejiang, China.
Long ShiZhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Zhejiang, China.
Hang MuZhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Zhejiang, China.
Wen-Bin OuZhejiang Provincial Key Laboratory of Silkworm Bioreactor and Biomedicine, College of Life Sciences, Zhejiang Sci-Tech University, Hangzhou, China.ORCID https://orcid.org/0000-0002-6311-9442
Jie PengWomen's Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
Ting-Ting LiDepartment of Geriatric Gastroenterology, Chinese People's Liberation Army General Hospital, Beijing, China.
Tianyi QinDepartment of Biology, Georgetown Preparatory School, North Bethesda, USA.
Hai-Meng ZhouZhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Zhejiang, China.
Xue-Qi FuCollege of Life Sciences, Jilin University, Changchun, China.
Xu-Hui LiZhejiang Provincial Key Laboratory of Applied Enzymology, Yangtze Delta Region Institute of Tsinghua University, Zhejiang, China.
Tsinghua University · CNJilin University · CNChinese People's Liberation Army · CNUniversity Prep · USWomen's Hospital, School of Medicine, Zhejiang University · CNZhejiang Sci-Tech University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase CK2 alpha (CK2α) is involved in the development of multiple malignancies. Overexpression of Y-box binding protein 1 (YBX1) is related to tumor proliferation, drug resistance, and poor prognosis. Studies have demonstrated that both CK2 and YBX1 could regulate the PI3K/AKT pathway. In addition, we predicted that CK2 might be the upstream kinase of YBX1 through the Human Protein Reference Database (HPRD). Herein, we hypothesize that CK2 may interact with YBX1 and they regulate the PI3K/AKT signaling pathway together. Expressions of CK2α and YBX1 in cancer cell lines were evaluated by immunoblotting. The results showed that CK2α could regulate the expression of YBX1 at the transcriptional level, which is dependent on its enzymatic activity. Synergistic effects of PI3K/AKT pathway inactivation could be observed through combined inhibition of CK2α and YBX1, and YBX1 was required for CK2α-induced PI3K/AKT pathway activation. Further results demonstrated that CK2α could interact with YBX1 and PI3K/AKT antagonist decreased cell resistance to doxorubicin induced by co-activation of CK2α and YBX1. These results indicated that combined inhibition of CK2α and YBX1 showed synergistic effects in inactivating the PI3K/AKT signaling pathway and may be one of the mechanisms involved in tumor growth and migration.

Indexed as

Casein Kinase IICell MovementCell ProliferationDoxorubicinDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHeLa CellsHep G2 CellsHumansNeoplasmsOncogene Protein v-aktPhosphatidylinositol 3-KinasesProtein BindingSignal TransductionY-Box-Binding Protein 1Casein Kinase IICSNK2A1 protein, humanDoxorubicinOncogene Protein v-aktPhosphatidylinositol 3-KinasesY-Box-Binding Protein 1YBX1 protein, humancancerCK2αYBX1

Identifiers

PMID31713447
PMCPMC6927700
OpenAlexW2986944126

What Socratic 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 Socratic graph.