Evidence map›Paper›PMID 26583330›Full record

ArticleCell death & disease2015

SOX4 contributes to the progression of cervical cancer and the resistance to the chemotherapeutic drug through ABCG2.

R Sun, B Jiang, H Qi, X Zhang, J Yang, J Duan, Y Li, G Li

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

39 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. CD133Heliyon · 2024
    Article
  11. SOX on tumors, a comfort or a constraint?Cell death discovery · 2024
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Multidrug efflux transporter ABCG2: expression and regulation.Cellular and molecular life sciences : CMLS · 2021
    Review
  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

8 authors at 4 institutions in 1 country.

R SunCancer Research Institute, Central South University, Changsha, China.
B JiangCancer Research Institute, Central South University, Changsha, China.
H QiThe Third Affiliated Hospital, Xinxiang Medical University, Xinxiang, China.
X ZhangCollaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine in Henan Province, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
J YangCollaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine in Henan Province, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
J DuanCollaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine in Henan Province, School of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Y LiCancer Research Institute, Central South University, Changsha, China.
G LiCancer Research Institute, Central South University, Changsha, China.
Xinxiang Medical University · CNCentral South University · CNMinistry of Education of the People's Republic of China · CNNational Health and Family Planning Commission · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SOX4, a member of the SOX (sex-determining region Y-related HMG box) transcription factor family, has been reported to be abnormally expressed in a wide variety of cancers, and to exert a pleiotropic function. However, its function in progression of cervical cancer (CC) remains unknown. In this study, we found that SOX4 was highly expressed in CC cells and tissues, and overexpression of SOX4 in CC CaSki cells enhanced tumor clone formation and cell proliferation, and accelerated cell cycle progress. Meanwhile, downregulation of SOX4 by shRNA in CaSki cells inhibited cell proliferation, and slowed cell cycle progress, indicating that SOX4 contributes to the development of CC. In addition, SOX4 overexpression by gene transfer reduced the sensitivity of CaSki cells in response to the chemotherapeutic drug cisplatin, and SOX4 downregulation by RNA interference increased the sensitivity of CaSki cells in response to cisplatin. Moreover, SOX4 overexpression upregulated multiple drug resistant gene ABCG2, and SOX4 downregulation inhibited ABCG2 expression. Taken together, these results suggested that SOX4 functions to modulate cancer proliferation by regulation of cell cycle, and inhibit cancer cell sensitivity to therapeutic drug via upregulation of ABCG2. Thus, SOX4 may be a target for CC chemotherapy.

Indexed as

AnimalsAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2Cell CycleCell ProliferationCisplatinDisease ProgressionDrug Resistance, NeoplasmEnoyl-CoA HydrataseFemaleHeLa CellsHeterograftsHumansMiceMice, Inbred BALB CABCG2 protein, humanAntineoplastic AgentsATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 2CisplatinEnoyl-CoA HydrataseNeoplasm ProteinsSOX4 protein, humanSOXC Transcription Factors

Identifiers

PMID26583330
PMCPMC4670919
OpenAlexW2179660271

What OpenQuestion holds

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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.