Evidence map›Paper›PMID 35227173›Full record

ArticleBioengineered2022

HOTAIR mediates cisplatin resistance in nasopharyngeal carcinoma by regulating miR-106a-5p/SOX4 axis.

Wei Cao, Yi Sun, Long Liu, Junwei Yu, Jiabiao Ji, Yatang Wang, Jianming Yang

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Osteosarcoma in a ceRNET perspective.Journal of biomedical science · 2024
    Review
  5. Review
  6. Review
  7. Review
  8. Non-coding RNA and drug resistance in head and neck cancer.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. 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

7 authors at 2 institutions in 1 country.

Wei CaoDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Yi SunDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Long LiuDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Junwei YuDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Jiabiao JiDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Yatang WangDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Jianming YangDepartment of Otorhinolaryngology, Head and Neck Surgery, The Second Hospital of Anhui Medical University, Hefei, China.
Second Hospital of Anhui Medical University · CNAnhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study explored the function and mechanisms of HOX transcript antisense RNA (HOTAIR) in the drug resistance of nasopharyngeal carcinoma (NPC). Quantitative PCR, Western blotting, MTT assay, flow cytometry, Transwell assay, and luciferase assay were performed. HOTAIR expression levels were upregulated in cisplatin (DDP)-resistant NPC tissues and cells. Knockdown of HOTAIR in DDP-resistant NPC cells increased cell sensitivity of DDP, as well as decreased cell viability, expression of chemoresistance-related proteins, migration and invasion, increased cell apoptosis. In addition, downregulation of microRNA 106a-5p (miR-106a-5p) expression and upregulation of SRY-box transcription factor 4 (SOX4) expression were observed in DDP-resistant NPC tissues and cells. MiR-106a-5p targets HOTAIR and SOX4; thus, silencing of HOTAIR significantly increased miR-106a-5p expression. The overexpression of miR-106a-5p significantly reversed the increase in SOX4 expression induced by HOTAIR lentivirus (Lv-HOTAIR). Knockdown of SOX4 reduced the drug resistance of DDP caused by the silencing of miR-106a-5p expression. In summary, HOTAIR enhanced DDP resistance in NPC cells by regulating the miR-106a-5p/SOX4 axis.

Indexed as

Nasopharyngeal CarcinomaAnimalsCell Line, TumorCisplatinDrug Resistance, NeoplasmHumansMiceMice, NudeMicroRNAsNasopharyngeal NeoplasmsNasopharynxRNA, Long NoncodingSOXC Transcription FactorsCisplatinHOTAIR long untranslated RNA, humanMicroRNAsMIRN106 microRNA, humanRNA, Long NoncodingSOX4 protein, humanSOXC Transcription Factorscisplatin resistanceHOTAIRmiR-106a-5p/SOX4 axisnasopharyngeal carcinoma

Identifiers

PMID35227173
PMCPMC8975274
OpenAlexW4214752193

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.