Evidence map›Paper›PMID 31949649›Full record

ArticleInternational journal of clinical and experimental pathology2018

MiR-106a-5p promotes 5-FU resistance and the metastasis of colorectal cancer by targeting TGFβR2.

Jian Liu, Yanqin Huang, Hongqian Wang, Denghai Wu

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

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 26% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  7. Apelin/APJ: Another Player in the Cancer Biology Network.International journal of molecular sciences · 2025
    Review
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  9. Review
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  13. Overview of miR-106a Regulatory Roles: from Cancer to Aging.Bioengineering (Basel, Switzerland) · 2023
    Review
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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

4 authors at 1 institution in 1 country.

Jian LiuDepartment of General Surgery, The Second Affiliated Hospital of Zhejiang Chinese Medical University (Xinhua Hospital of Zhejiang Province) Hangzhou, China.
Yanqin HuangCancer Institute, Second Affiliated Hospital, College of Medicine, Zhejiang University Hangzhou, China.
Hongqian WangDepartment of General Surgery, The Second Affiliated Hospital of Zhejiang Chinese Medical University (Xinhua Hospital of Zhejiang Province) Hangzhou, China.
Denghai WuDepartment of General Surgery, The Second Affiliated Hospital of Zhejiang Chinese Medical University (Xinhua Hospital of Zhejiang Province) Hangzhou, China.
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) is the third leading cause of cancer-related deaths. 5-Fluorouracil (5-FU)-based chemotherapy has always been the first-line treatment. However, development of 5-FU resistance seriously affects its curative effect. The aim of this study was to elucidate the molecular mechanisms of 5-FU resistance through miR-106a-5p in CRC.

methodsColorectal cancer tissues were collected to analyze miR-106a-5p and TGFβR2 expressions by qPCR. Functional experiments for evaluating cell survival and metastasis were conducted to observe the biological effects of miR-106a-5p and TGFβR2. The cell survival rate was calculated using an MTT assay; the metastasis was confirmed with a Transwell invasion assay and Western blotting, which we used to measure the expression levels of the epithelial-mesenchymal transition (EMT) markers E-cadherin and vimentin. The combination of miR-106a to TGFβR2 was predicted using

resultsMiR-106a-5p was up-regulated and TGFβR2 was down-regulated in 5-FU resistant CRC tissues and HT-29 cells. MiR-106a-5p promoted cell survival and suppressed the apoptosis rate and caspase 3 activity. Additionally, cell invasion was promoted by miR-106a-5p overexpression in the HT-29 cells and was inhibited by miR-106a-5p knockdown in the 5-FU resistant HT-29 cells; miR-106a-5p overexpression contributed to migration by increasing vimentin expression and by decreasing E-cadherin expression in the HT-29 cells; miR-106a-5p functioned by directly binding to TGFβR2. The TGFβR2 knockdown conferred chemoresistance of 5-FU and metastasis in 5-FU resistant HT-29 cells, and TGFβR2 overexpression reduced cell survival, invasion numbers, vimentin expression, and increased the cell apoptosis rate and caspase 3 activity in 5-FU resistant HT-29 cells. Also, miR-106a-5p negatively regulated TGFβR2 in a linear correlation way in the CRC tissues.

conclusionThe up-regulation of miR-106a-5p contributes to the pathomechanism of colorectal cancer by promoting 5-FU resistance and metastasis via inhibiting target TGFβR2. Our findings provide new promising ways for the clinical application of the TGFβR2-miR-106a axis in clinical chemotherapy for 5-FU resistant colorectal cancer.

Indexed as

5-FU resistancecolorectal cancermetastasisMiR-106a-5pTGFβR2

Identifiers

PMID31949649
PMCPMC6963073
OpenAlexW3004966238

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.