Evidence map›Paper›PMID 31894287›Full record

ArticleOncology reports2020

lncRNA XIST promotes the progression of laryngeal squamous cell carcinoma by sponging miR‑144 to regulate IRS1 expression.

Chang-Lei Cui, Yi-Ning Li, Xiang-Yan Cui, Xin Wu

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Long non-coding RNA XIST: a novel oncogene in multiple cancers.Molecular medicine (Cambridge, Mass.) · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Biological Function of Long Non-coding RNA (LncRNA) Xist.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Chang-Lei CuiDepartments of Anesthesiology, The First Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Yi-Ning LiDepartment of Otorhinolaryngology‑Head and Neck Surgery, The First Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Xiang-Yan CuiDepartment of Otorhinolaryngology‑Head and Neck Surgery, The First Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
Xin WuDepartment of Otorhinolaryngology‑Head and Neck Surgery, The First Hospital of Jilin University, Changchun, Jilin 130033, P.R. China.
First Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The initiation and development of several types of cancer have been linked to long non‑coding RNA (lncRNA) X inactive‑specific transcript (XIST). Yet, the pattern of expression, function, as well as the molecular mechanism underlying XIST in laryngeal squamous cell carcinoma (LSCC) lack characterization. Therefore, the present study aimed to determine the function and putative mechanism of XIST in the development of LSCC. It was revealed that the level of XIST was significantly higher in LSCC tissues that were associated with advanced Tumor‑Node‑Metastasis (TNM) stage and the presence of lymph node metastasis. Furthermore, the ability of human LSCC TU212 cells to proliferate, form colonies, migrate and invade was significantly suppressed, while cell apoptosis was significantly increased following knockdown of XIST. Further investigation revealed that XIST knockdown increased the expression of microRNA‑144 (miR‑144) by acting as an endogenous sponge of miR‑144. Inhibition of miR‑144 caused a partial reversal of the inhibitory effects mediated following depletion of XIST in LSCC cells. Moreover, an miR‑144 target called insulin receptor substrate 1 (IRS1) was significantly decreased by XIST depletion in LSCC cells. IRS1 expression was positively correlated with XIST expression in LSCC tissues. In addition, knockdown of XIST impaired tumor growth in vivo by regulating the miR‑144/IRS1 axis. The present study demonstrated that the progression of LSCC is promoted by XIST sponging miR‑144 to regulate IRS1 expression, suggesting that XIST can serve as a putative target in the therapy of LSCC.

Indexed as

AnimalsCarcinoma, Squamous CellCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansInsulin Receptor Substrate ProteinsLaryngeal NeoplasmsMaleMicroRNAsMiddle AgedNeoplasm StagingPrognosisRNA, Long NoncodingInsulin Receptor Substrate ProteinsIRS1 protein, humanMicroRNAsMIRN144 microRNA, humanRNA, Long NoncodingXIST non-coding RNA

Identifiers

PMID31894287
PMCPMC6967080
OpenAlexW2995477771

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.