Evidence map›Paper›PMID 27900563›Full record

ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016

LncRNA HOTAIR promotes cisplatin resistance in gastric cancer by targeting miR-126 to activate the PI3K/AKT/MRP1 genes.

Jin Yan, Yini Dang, Shiyu Liu, Yifeng Zhang, Guoxin Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 1 pooled it
9.4field-weighted citation impact, top 1% 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

89 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Therapeutic opportunities in EBV-positive gastric cancer subtypes.Therapeutic advances in medical oncology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Cellular and Molecular Mechanisms of Chemoresistance for Gastric Cancer.International journal of general medicine · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

29 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Jin YanDepartment of Gastroenterology, The First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, Gulou District, Nanjing, Jiangsu, 210000, China.
Yini DangDepartment of Gastroenterology, The First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, Gulou District, Nanjing, Jiangsu, 210000, China.
Shiyu LiuDepartment of Gastroenterology, The First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, Gulou District, Nanjing, Jiangsu, 210000, China.
Yifeng ZhangDepartment of Gastroenterology, The First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, Gulou District, Nanjing, Jiangsu, 210000, China.
Guoxin ZhangDepartment of Gastroenterology, The First Affiliated Hospital with Nanjing Medical University, 300 Guangzhou Road, Gulou District, Nanjing, Jiangsu, 210000, China. guoxinz@njmu.edu.cn.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered expression of long noncoding RNAs (lncRNAs) has shown to associate with human cancer development and progression and drug resistance. LncRNA HOX antisense intergenic RNA (HOTAIR) regulates chromatin state and highly expressed in various human cancers. This study analyzed HOTAIR expression in gastric cancer cells and tissues and then assessed the effects of HOTAIR on modulation of gastric cancer cell sensitivity to cisplatin and the underlying molecular events. The data showed that HOTAIR was significantly upregulated in cisplatin-resistant gastric cancer cells and tissues compared with control cells and noncancerous gastric tissues. Overexpression of HOTAIR enhanced gastric cancer cell proliferation, promoted cell cycle G1/S transition, but decreased tumor cell apoptosis. Furthermore, HOTAIR was shown to directly bind to and inhibit miR-126 expression and then to promote VEGFA and PIK3R2 expression and activate the PI3K/AKT/MRP1 pathway. In conclusion, the data demonstrated that high HOTAIR expression acted as a competitive endogenous RNA to promote cisplatin resistance in gastric cancer. Further study will evaluate HOTAIR expression as a biomarker to predict treatment response of cisplatin and explore inhibition of HOTAIR expression as a novel strategy for anti-cisplatin resistance in human gastric cancer.

Indexed as

Cisplatin resistanceGastric cancerHOTAIRmiR-126PI3K/AKT

Identifiers

PMID27900563
OpenAlexW2558855014

What OpenQuestion holds

Textmetadata
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.