Evidence map›Paper›PMID 33585440›Full record

ArticleFrontiers in cell and developmental biology2020

Exosomal Long Non-coding RNA HOTTIP Increases Resistance of Colorectal Cancer Cells to Mitomycin via Impairing MiR-214-Mediated Degradation of KPNA3.

Xijuan Chen, Yingqiang Liu, Qinglan Zhang, Baoxing Liu, Yan Cheng, Yonglei Zhang, Yanan Sun, Junqi Liu, Hong Gen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.

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  19. Extracellular Vesicles in Cancer Drug Resistance: Roles, Mechanisms, and Implications.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Review
  20. Tumor-derived exosomal non-coding RNAs as diagnostic biomarkers in cancer.Cellular and molecular life sciences : CMLS · 2022
    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

9 authors at 2 institutions in 1 country.

Xijuan ChenDepartment of Radiation Oncology, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Yingqiang LiuDepartment of General Surgery, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Qinglan ZhangDepartment of Hematology, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Baoxing LiuDepartment of Chest Surgery, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Yan ChengDepartment of Gynecology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Yonglei ZhangDepartment of General Surgery, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Yanan SunDepartment of Radiation Oncology, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Junqi LiuDepartment of Radiation Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Hong GenDepartment of Radiation Oncology, The Affiliated Tumor Hospital of Zhengzhou University, Zhengzhou, China.
Zhengzhou University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been reported that long non-coding RNA HOXA distal transcript antisense RNA (lncRNA HOTTIP) functions as a tumor promoter in colorectal cancer (CRC). Hence, we paid attention to exploring whether exosomes could carry lncRNA HOTTIP to affect the mitomycin resistance in CRC and to identify the underlying mechanisms. High expression of HOTTIP was detected in mitomycin-resistant CRC cells. Inhibition of HOTTIP reduced the mitomycin resistance. In the co-culture system of mitomycin-resistant cells or their derived exosomes with CRC cells, the HOTTIP was found to be transferred into the parental cells via extracellular vesicles (EVs) secreted from mitomycin-resistant cells and to contribute to the mitomycin resistance. Based on the bioinformatics databases, possible interaction network of HOTTIP, microRNA-214 (miR-214) and Karyopherin subunit alpha 3 (KPNA3) in CRC was predicted, which was further analyzed by dual-luciferase reporter, RNA binding protein immunoprecipitation and RNA pull-down assays. As HOTTIP down-regulated miR-214 to elevate the KPNA3 expression, HOTTIP enhanced the mitomycin resistance through impairing miR-214-dependent inhibition of KPNA3. Finally, HOTTIP was suggested as an independent factor predicting mitomycin response in patients with CRC. Those data together confirmed the promotive effects of EV-carried HOTTIP on the mitomycin resistance, while targeting HOTTIP might be a promising strategy overcoming drug resistance in CRC.

Indexed as

colorectal cancerdrug resistanceexosomesHOXA distal transcript antisense RNAKPNA3long non-coding RNAmicroRNA-214

Identifiers

PMID33585440
PMCPMC7876302
OpenAlexW3123711776

What OpenQuestion holds

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Registered trials

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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.