Evidence map›Paper›PMID 30293547›Full record

ArticleBMB reports2018

Overexpression of CXCL2 inhibits cell proliferation and promotes apoptosis in hepatocellular carcinoma.

Jun Ding, Kangdi Xu, Jie Zhang, Bingyi Lin, Yubo Wang, Shengyong Yin, Haiyang Xie, Lin Zhou, Shusen Zheng

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.7field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Bioinformatic Analysis of the CXCR2 Ligands in Cancer Processes.International journal of molecular sciences · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  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

9 authors at 3 institutions in 1 country.

Jun DingDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital School of Medicine, Zhejiang University; Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health; Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences; Key Laboratory of Organ Transplantation, Hangzhou, Zhejiang 310003, P.R.China.
Kangdi XuDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital School of Medicine, Zhejiang University; Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health; Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences; Key Laboratory of Organ Transplantation, Hangzhou, Zhejiang 310003, P.R.China.
Jie ZhangDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital School of Medicine, Zhejiang University; Department of Hepatobiliary Surgical, First Hospital of Jiaxing, Jiaxing, Zhejiang 314000, P.R.China.
Bingyi LinDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital School of Medicine, Zhejiang University; Collaborative Innovation Center for Diagnosis treatment of infectious diseases, Hangzhou, Zhejiang 310003, P.R.China.
Yubo WangDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital School of Medicine, Zhejiang University; Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health; Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences, Hangzhou, Zhejiang 310003, P.R.China.
Shengyong YinKey Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health; Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences; Key Laboratory of Organ Transplantation, Hangzhou, Zhejiang 310003, P.R.China.
Haiyang XieKey Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health; Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences; Key Laboratory of Organ Transplantation, Hangzhou, Zhejiang 310003, P.R.China.
Lin ZhouKey Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences; Key Laboratory of Organ Transplantation, Hangzhou, Zhejiang 310003; Collaborative Innovation Center for Diagnosis treatment of infectious diseases, Hangzhou, Zhejiang 310003, P.R.China.
Shusen ZhengDivision of Hepatobiliary and Pancreatic Surgery, Department of Surgery First Affiliated Hospital School of Medicine, Zhejiang University; Key Laboratory of Combined Multi-organ Transplantation, Ministry of Public Health; Key Laboratory of the Diagnosis and Treatment of Organ Transplantation, Chinese Academy of Medical Sciences; Key Laboratory of Organ Transplantation, Hangzhou, Zhejiang 310003; Collaborative Innovation Center for Diagnosis treatment of infectious diseases, Hangzhou, Zhejiang 310003, P.R.China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNFirst Hospital of Jiaxing · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C-X-C motif chemokine ligand 2 (CXCL2) is a small secreted protein that exhibits a structure similar to the proangiogenic subgroup of the CXC chemokine family. Recently, accumulating evidence suggests that chemokines play a pivotal role in cancer progression and carcinogenesis. We examined the expression levels of 7 types of ELR+ CXCLs messenger RNA (mRNA) in 264 clinical samples. We found that CXCL2 expression was stably down-regulated in 94% of hepatocellular carcinoma (HCC) specimens compared with paired adjacent normal liver tissues and some HCC cell lines. Moreover, CXCL2 overexpression profoundly attenuated HCC cell proliferation and growth and induced apoptosis in vitro. In animal studies, we found that overexpressing CXCL2 by lentivirus also apparently inhibited the size and weight of subcutaneous tumours in nude mice. Furthermore, we demonstrated that CXCL2 induced HCC cell apoptosis via both nuclear and mitochondrial apoptosis pathways. Our results indicate that CXCL2 negatively regulates the cell cycle in HCC cells via the ERK1/2 signalling pathway. These results provide new insights into HCC and may ultimately lead to the discovery of innovative therapeutic approaches of HCC. [BMB Reports 2018; 51(12): 630-635].

Indexed as

ApoptosisCell ProliferationAnimalsCarcinoma, HepatocellularCell Cycle CheckpointsCell Line, TumorChemokine CXCL2Down-RegulationFemaleHumansLiver NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMiddle AgedChemokine CXCL2CXCL2 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3RNA, Small Interfering

Identifiers

PMID30293547
PMCPMC6330937
OpenAlexW2907695702

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.