Evidence map›Paper›PMID 32323786›Full record

ArticleOncology reports2020

Catalpol‑mediated microRNA‑34a suppresses autophagy and malignancy by regulating SIRT1 in colorectal cancer.

Peng-Fei Qiao, Lei Yao, Zhao-Lin Zeng

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
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. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  6. A Study of the Fruits ofAntioxidants (Basel, Switzerland) · 2025
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  11. The role of SIRT1 in the development of gastrointestinal tumors.Frontiers in cell and developmental biology · 2025
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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

3 authors at 2 institutions in 1 country.

Peng-Fei QiaoDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Lei YaoDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Zhao-Lin ZengDepartment of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Second Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is one of the most common digestive tract tumors worldwide. Catalpol exerts inhibitory effects on the progression of several cancer types by regulating microRNAs (miRs). However, the precise role and carcinostatic mechanism of catalpol on CRC cells are poorly understood which limits the application of catalpol treatment. In the present study, miR‑34a and sirtuin 1 (SIRT1) expression levels were detected in CRC tissues and CRC cell lines by RT‑qPCR. Computational software analysis, luciferase assays and western blotting were used to demonstrate the downstream target of miR‑34a in CRC cells. Effects of catalpol on cell viability, apoptosis, autophagic flux and the miR‑34a/SIRT1 axis in the CRC cells were assessed by CCK‑8 assay, flow cytometry, electron microscopy and western blotting, respectively. Whether the miR‑34a/SIRT1 axis participated in catalpol‑mediated autophagy and apoptosis was investigated. The effects of catalpol on the miR‑34a/SIRT1 axis and malignant behavior were evaluated in a rat model of azoxymethane (AOM)‑induced CRC. It was revealed that miR‑34a expression levels were significantly decreased while SIRT1 was overexpressed in most of the CRC tissues and all the CRC cell lines. Clinically, a low level of miR‑34a was correlated with poor clinicopathological characteristics in CRC patients. Catalpol reduced cell viability, suppressed autophagy, promoted apoptosis, and regulated the expression of SIRT1 by inducing miR‑34a in vitro and in vivo. The autophagy‑inhibiting effect of catalpol may be a mechanism to promote apoptosis of CRC cells. miR‑34a mimic transfection resulted in autophagy‑suppressive activity similar to that of catalpol, while the miR‑34a inhibitor attenuated the antiautophagic effects of catalpol. In conclusion, miR‑34a is involved in regulating catalpol‑mediated autophagy and malignant behavior by directly inhibiting SIRT1 in CRC.

Indexed as

AutophagyAgedAnimalsApoptosisAzoxymethaneCarcinogensCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsColorectal NeoplasmsDisease Models, AnimalDrugs, Chinese HerbalFemaleGene Expression Regulation, NeoplasticHumansAzoxymethaneCarcinogenscatalpolDrugs, Chinese HerbalIridoid GlucosidesMicroRNAsMIRN34 microRNA, humanSIRT1 protein, humanSirtuin 1autophagycatalpolcolorectal cancermiR-34aSIRT1

Identifiers

PMID32323786
PMCPMC7057773
OpenAlexW3004698906

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.