Evidence map›Paper›PMID 32757663›Full record

ArticleCell transplantation

HOTAIR Promotes Cisplatin Resistance of Osteosarcoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/STAT3 Axis.

Jiankuo Guo, Dongmei Dou, Tianlun Zhang, Bo Wang

Open access · goldAbstract read
In one paragraph

Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Osteosarcoma in a ceRNET perspective.Journal of biomedical science · 2024
    Review
  10. Role of Epigenetics for the Efficacy of Cisplatin.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Review
  13. Overview of miR-106a Regulatory Roles: from Cancer to Aging.Bioengineering (Basel, Switzerland) · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

4 authors at 4 institutions in 1 country.

Jiankuo GuoDepartment of Orthopedics, Huaihe Hospital of Henan University, Kaifeng, Henan Province, China.
Dongmei DouInstitute for Slow Disease Risk Assessment, Henan University, Kaifeng, Henan Province, China.
Tianlun ZhangSchool of Information and Communication Engineering, University of Electronic Science and Technology of China, Chengdu, Sichuan Province, China.
Bo WangDepartment of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China.ORCID 0000-0003-1304-2413
Henan University · CNHenan University Huaihe Hospital and Huaihe Clinical Institute · CNTongji Hospital · CNUniversity of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteosarcoma (OS) is a common primary malignant bone tumor among adolescences, and the emergence of multidrug resistance poses a huge challenge for clinical treatment of OS. LncRNA HOTAIR (HOX antisense intergenic RNA) has been reported to be associated with many malignancies, including OS. However, the underlying mechanisms of HOTAIR involved in drug resistance in OS are obscure. Our study showed that HOTAIR was upregulated in cisplatin (DDP)-resistant OS tissues and cells. HOTAIR knockdown decreased the DDP resistance, drug resistance-related gene expression, cell proliferation, and invasion and promoted apoptosis of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells. Mechanism researches displayed that miR-106a-5p was downregulated in DDP-resistant OS tissues and cells. MiR-106a-5p directly bound with HOTAIR and was regulated by HOTAIR. Moreover, STAT3 was inhibited by miR-106a-5p at a post-transcriptional level, and the transfection of miR-106a-5p reversed the upregulation of STAT3 caused by HOTAIR overexpression. The increase or decrease of miR-106a-5p suppressed the effect of HOTAIR upregulation or downregulation on DDP resistance, cell proliferation, invasion, and apoptosis of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells. What's more, the transfection of STAT3 siRNA reversed the decrease of DDP resistance, cell proliferation, and invasion and rescued the increase of apoptosis induced by miR-106a-5p inhibition. These data suggested that HOTAIR enhanced DDP resistance of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells by affecting cell proliferation, invasion, and apoptosis via miR-106a-5p/STAT3 axis.

Indexed as

AdolescentAdultApoptosisBone NeoplasmsCell ProliferationChildChild, PreschoolCisplatinHumansMicroRNAsNeoplasm InvasivenessOsteosarcomaRNA, Long NoncodingSTAT3 Transcription FactorYoung AdultCisplatinHOTAIR long untranslated RNA, humanMicroRNAsMIRN106 microRNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription Factorcisplatin resistanceLncRNA HOTAIRmiR-106a-5p/STAT3 axisosteosarcoma

Identifiers

PMID32757663
PMCPMC7563817
OpenAlexW3047106446

What Socratic 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 Socratic graph.