Evidence map›Paper›PMID 33948353›Full record

ArticleAmerican journal of cancer research2021

AKIP1 promotes glioblastoma viability, mobility and chemoradiation resistance via regulating CXCL1 and CXCL8 mediated NF-κB and AKT pathways.

Dayong Han, Na Zhang, Shu Zhao, Huailei Liu, Xiaoxiong Wang, Mingchun Yang, Shengtao Wang, Yue Li, Zhanwen Liu, Lei Teng

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. The Significance of CXCL1 in Cancer: An Overview of Molecular Mechanisms.International journal of molecular sciences · 2026
    Review
  3. Therapeutic Potential ofInternational journal of general medicine · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. TGFβ1 induces CXCL1 to promote stemness features in lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 1 institution in 1 country.

Dayong HanDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Na ZhangDepartment of Laboratory Diagnostics, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Shu ZhaoDepartment of Emergency Internal Medicine, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Huailei LiuDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Xiaoxiong WangDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Mingchun YangDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Shengtao WangDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Yue LiDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Zhanwen LiuDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Lei TengDepartment of Neurosurgery, The First Clinical College of Harbin Medical University Nangang District, Harbin 150001, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to investigate the interaction of A-kinase-interacting protein 1 (AKIP1) with C-X-C motif chemokine ligand (CXCL)1, CXCL2, CXCL8, and their effects on regulating glioblastoma multiforme (GBM) malignant behaviors. AKIP1 expression was modified by pcDNA and pGPH1 vectors in U-87 MG and U-251 MG cells. Subsequently, multiple compensative experiments were conducted via adding CXCL1, CXCL2 and CXCL8 in the pGPH1-AKIP1 (AKIP1 knockdown) transfected U-87 MG and U-251 MG cells, respectively. Furthermore, AKIP1, CXCL1/2/8 expressions in 10 GBM and 10 low-grade glioma (LGG) tumor samples were detected. AKIP1 was elevated in various GBM cell lines compared to normal human astrocytes. AKIP1 overexpression promoted U-87 MG and U-251 MG cell proliferation and invasion while inhibited apoptosis; and it enhanced chemoresistance to temozolomide (but not cisplatin) and radiation resistance; then AKIP1 knockdown showed the opposite effects. Meanwhile, AKIP1 positively regulated CXCL1/2/8, NF-κB pathway, AKT pathway and PD-L1 expression. Further multiple compensative experiments uncovered that CXCL1 and CXCL8 promoted proliferation, invasion, chemoradiation resistance, NF-κB pathway, AKT pathway and PD-L1 expression in U-87 MG and U-251 MG cells, also in pGPH1-AKIP1 (AKIP1 knockdown) transfected U-87 MG and U-251 MG cells; although CXCL2 exhibited similar treads, but its effect was much weaker. Besides, NF-κB pathway inhibitor and AKT pathway inhibitor attenuated the effect of CXCL1&CXCL8 on promoting GBM cell malignant behaviors. Clinically AKIP1 and CXCL1/8 were elevated in GBM compared to LGG tumor samples, and they were inter-correlated. AKIP1 promotes GBM viability, mobility and chemoradiation resistance via regulating CXCL1 and CXCL8 mediated NF-κB and AKT pathways.

Indexed as

A-kinase-interacting protein 1chemoradiation resistanceC-X-C motif chemokine ligandglioblastoma multiformeNF-κB and AKT pathways

Identifiers

PMID33948353
PMCPMC8085855
OpenAlexW3158201979

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.