Evidence map›Paper›PMID 26206082›Full record

ArticleScientific reports2015

Flotillin-2 promotes metastasis of nasopharyngeal carcinoma by activating NF-κB and PI3K/Akt3 signaling pathways.

Jie Liu, Wei Huang, Caiping Ren, Qiuyuan Wen, Weidong Liu, Xuyu Yang, Lei Wang, Bin Zhu, Liang Zeng, Xiangling Feng and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.6field-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

35 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. HDAC6-mediated deacetylation of FLOT2 maintains stability and tumorigenic function of FLOT2 in nasopharyngeal carcinoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. International journal of biological sciences · 2023
    Article
  8. Function of AXL and molecular mechanisms in regulation of nasopharyngeal carcinoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. SIRT6 inhibits metastasis by suppressing SNAIL expression in nasopharyngeal carcinoma cells.International journal of clinical and experimental pathology · 2021
    Article
  17. Article
  18. Review
  19. Article
  20. Flotillin membrane domains in cancer.Cancer metastasis reviews · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 1 country.

Jie LiuCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Wei HuangCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Caiping RenCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Qiuyuan WenCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Weidong LiuCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Xuyu YangCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Lei WangCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Bin ZhuCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Liang ZengDepartment of Pathology, Hunan Cancer Hospital, Changsha, Hunan, P. R. China.
Xiangling FengCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Chang ZhangCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Huan ChenCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Wei JiaCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Lihua ZhangCancer Research Institute, Collaborative Innovation Center for Cancer Medicine, Key Laboratory for Carcinogenesis of Chinese Ministry of Health, School of Basic Medical Science, Central South University, Xiangya Road 110, 410078, Changsha, Hunan, P. R. China.
Xiaomeng XiaDepartment of Gynaecology and Obstetrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, P. R. China.
Yuxiang ChenHepatobiliary &Enteric Surgery Research Center, Xiangya Hospital, Central South University, Changsha, Hunan, P. R. China.
Central South University · CNHunan Cancer Hospital · CNSecond Xiangya Hospital of Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid raft proteins have been confirmed to be important in cell signal transduction. Some reports have shown that the aberrant expression of lipid raft proteins is associated with malignant phenotypes in some cancers. However, the role of the lipid raft protein flotillin-2 (Flot-2) in nasopharyngeal carcinoma (NPC) remains to be comprehensively characterized. Here, overexpression of Flot-2 in NPC tissues and cell lines was detected by immunostaining, and Flot-2 expression was found to be positively associated with NPC metastasis. Furthermore, inhibiting Flot-2 expression impaired the malignancy of the highly metastatic NPC cell line 5-8F by constraining its growth and proliferation, mobility and migration, and decreasing the capacity of 5-8F cells to metastasize in nude mice. In contrast, forced overexpression of Flot-2 increased the malignancy of 6-10B, a non-metastatic NPC cell line that weakly expresses Flot-2. Moreover, in 5-8F-shFlot-2 cells, which have inhibited Flot-2 expression, the NF-κB and PI3K/Akt3 pathways were inactivated. Subsequently, MMPs expression were decreased, and Foxo1 activity was increased. In addition, enhanced NF-κB and PI3K/Akt3 activities were observed in Flot-2 overexpressing 6-10B cells. Thus, Flot-2 exerts a pro-neoplastic role in NPC and is involved in tumor progression and metastasis. Moreover, Flot-2 exerts its role through NF-κB and PI3K/Akt3 signaling.

Indexed as

Signal TransductionAnimalsCarcinomaCell Line, TumorHeterograftsHumansMembrane ProteinsMiceMice, NudeNasopharyngeal CarcinomaNasopharyngeal NeoplasmsNeoplasm MetastasisNeoplasm TransplantationNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAKT3 protein, humanflotillinsMembrane ProteinsNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID26206082
PMCPMC4648439
OpenAlexW2410155416

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LicenceCC BY
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Registered trials

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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.