Evidence map›Paper›PMID 30267476›Full record

ArticleCancer medicine2018

GNA13 promotes tumor growth and angiogenesis by upregulating CXC chemokines via the NF-κB signaling pathway in colorectal cancer cells.

Zhongqiang Zhang, Xiao Tan, Jing Luo, Beibei Cui, Sanlin Lei, Zhongzhou Si, Liangfang Shen, Hongliang Yao

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.8field-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

36 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. GRespiratory research · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Retraction · 2023-09-19Duplication of/in Image · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/5C9C5EA48DC2B3E7004D23591188DE
  • Retracted
5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Zhongqiang ZhangDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Xiao TanDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Jing LuoDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Beibei CuiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Sanlin LeiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Zhongzhou SiDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Liangfang ShenDepartment of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Hongliang YaoDepartment of General Surgery, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID 0000-0002-8085-3876
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GNA13 has been found overexpressed in various types of cancer, which is related to tumor metastasis and progression. However, the biological functions of GNA13 in colorectal cancer (CRC) progression remain unclear. This study aimed to explore the role of GNA13 in CRC and investigate the mechanism of how GNA13 promotes tumor growth. Interestingly, our findings showed that GNA13 is commonly upregulated in CRC, where these events are associated with a worse histologic grade and poor survival. Increased expression levels of GNA13 promoted cell growth, migration, invasion, and epithelial-mesenchymal transition, whereas GNA13 silencing abrogated these malignant phenotypes. In addition, overexpressing GNA13 in cancer cells increased the levels of the chemokines CXCL1, CXCL2, and CXCL4, which contributed to CRC proliferation and colony formation. Moreover, our mechanistic investigations suggest that the NF-κB/p65 signaling pathway was activated by the increase in GNA13 levels. Inhibiting the NF-κB/p65 pathway with an inhibitor decreased GNA13-induced migration, invasion and CXCL chemokine level increases, indicating the critical role of NF-κB/p65 signaling in mediating the effects of GNA13 in CRC. Together, these results demonstrate a key role of GNA13 overexpression in CRC that contributes to malignant behavior in cancer cells, at least in part through stimulating angiogenesis and increasing the levels of the NF-κB-dependent chemokines CXCL1, CXCL2, and CXCL4.

Indexed as

Signal TransductionUp-RegulationAnimalsCell ProliferationChemokines, CXCColorectal NeoplasmsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGTP-Binding Protein alpha Subunits, G12-G13HCT116 CellsHT29 CellsHumansMiceNeoplasm GradingNeoplasm TransplantationNF-kappa BChemokines, CXCGNA13 protein, humanGTP-Binding Protein alpha Subunits, G12-G13NF-kappa BCRCCXCL chemokinesGNA13NF-κB

Identifiers

PMID30267476
PMCPMC6246959
OpenAlexW2893276870

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.