Evidence map›Paper›PMID 29328404›Full record

ArticleOncology reports2018

Chronic oxymatrine treatment induces resistance and epithelial‑mesenchymal transition through targeting the long non-coding RNA MALAT1 in colorectal cancer cells.

Yibai Xiong, Jun Wang, Huirong Zhu, Lingshuang Liu, Yi Jiang

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncology reports, 2018. 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 It has been retracted, and should not be counted.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 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Yibai XiongDepartment of Oncology, Longhua Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200021, P.R. China.
Jun WangDepartment of Anorectal Surgery, First Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang 310000, P.R. China.
Huirong ZhuShanghai University of Traditional Chinese Medicine, Shanghai 200021, P.R. China.
Lingshuang LiuDepartment of Oncology, Longhua Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200021, P.R. China.
Yi JiangDepartment of Oncology, Longhua Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai 200021, P.R. China.
Shanghai University of Traditional Chinese Medicine · CNFirst Affiliated Hospital Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major reason for colorectal cancer (CRC) chemoresistance is the enhanced migration and invasion of cancer cells, such as the cell acquisition of epithelial-mesenchymal transition (EMT). Long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been considered as a pro-oncogene in multiple cancers. However, the precise functional mechanism of lncRNA MALAT1 in chemoresistance and EMT is not well known. In the present study, we focused on the effect of oxymatrine on CRC cells and further investigated the role of MALAT1 in oxymatrine-induced resistance and EMT process. The human CRC cell line HT29 was exposed to increasing doses of oxymatrine to establish stable cell lines resistant to oxymatrine. The established HT29 oxymatrine resistant cells showed an EMT phenotype including specific morphologic changes, enhanced migratory and invasive capacity, and downregulation of E-cadherin protein expression. Subsequently, high-throughput HiSeq sequencing and RT-qPCR showed that lncRNA MALAT1 was significantly upregulated in the oxymatrine resistant cells (P<0.01), while knockdown of MALAT1 partially reversed the EMT phenotype in HT29 resistant cells. Furthermore, oxymatrine treatment suppressed the migration and invasion ability of CRC cells, however, this effect was significantly reversed by overexpression of MALAT1. Finally, we investigated the clinical role of MALAT1 and found that high lncRNA MALAT1 expression level is associated with poor prognosis in CRC patients receiving oxymatrine treatment (P<0.01). In conclusion, we demonstrate that lncRNA MALAT1 is a stimulator for oxymatrine resistance in CRC and it may provide therapeutic and prognostic information for CRC patients.

Indexed as

AdenocarcinomaAdultAgedAlkaloidsAntigens, CDAntiviral AgentsApoptosisBiomarkers, TumorCadherinsCase-Control StudiesCell MovementCell ProliferationColorectal NeoplasmsDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleAlkaloidsAntigens, CDAntiviral AgentsBiomarkers, TumorCadherinsCDH1 protein, humanMALAT1 long non-coding RNA, humanMatrinesoxymatrineQuinolizinesRNA, Long Noncoding

Identifiers

PMID29328404
PMCPMC5802036
OpenAlexW2783408209

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.