Evidence map›Paper›PMID 32190086›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2020

Aloe-Emodin Induces Breast Tumor Cell Apoptosis through Upregulation of miR-15a/miR-16-1 That Suppresses BCL2.

Xuefeng Jiang, Yusheng Liu, Guijuan Zhang, Shujun Lin, Jieyan Wu, Xianxin Yan, Yi Ma, Min Ma

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

Article in Evidence-based complementary and alternative medicine : eCAM, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Xuefeng JiangCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.
Yusheng LiuCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.
Guijuan ZhangThe First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, China.
Shujun LinCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.
Jieyan WuCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.
Xianxin YanCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.
Yi MaInstitute of Biomedicine and Department of Cellular Biology, Jinan University, Guangzhou, Guangdong 510632, China.
Min MaCollege of Traditional Chinese Medicine, Jinan University, Guangzhou, Guangdong 510632, China.ORCID https://orcid.org/0000-0003-3602-6846
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeAloe-emodin (AE) is a natural compound derived from aloe vera and palmatum rhubarb and shows anticancer activities in various cancers. Bcl-2 family is the main regulator of cell death or cell survival. This study describes the effects of AE on proliferation of breast tumor (BT) cells.

methodsMCF-10A, MCF-10AT, MCF-7, and MDA-MB-231 cell lines were exposed to AE. Cell proliferation and apoptosis were assessed by CCK-8 and flow cytometry. Protein levels were measured by Western blotting. The levels of mRNA and miRNA were examined by RT-PCR. Bioinformatics was applied to screen miRNAs that bind to 3'-UTR of mRNA.

resultsThe results showed that AE selective activity inhibited the proliferation and induced apoptosis of MCF-10AT and MCF-7 cells but exhibited no significant inhibition in MCF10A and MDA-MB-231 cells. Mechanistically, AE dose-dependently decreased the protein expression of Bcl-2 and Bcl-xl, while it increased Bax protein expression in MCF-10AT and MCF-7 cells. The levels of Bcl-xl and Bax mRNA were altered by AE treatment, which was consistent with the protein expression results. However, Bcl-2 mRNA levels were not affected in either cell line, suggesting that AE may modulate the protein translation of Bcl-2 through miRNAs. In all candidate miRNAs that bind to 3'-UTR of Bcl-2, miR-15a and miR-16-1 were dose-dependently downregulated by AE. Moreover, inhibition of miR-15a/16-1 could eliminate the inhibition of MCF-10AT and MCF-7 cells growth by AE and could reverse the downregulation of AE-induced Bcl-2 protein level.

conclusionOur research provides an important basis that AE induces BT cell apoptosis through upregulation of miR-15a/miR-16-1 that suppresses BCL2.

Identifiers

PMID32190086
PMCPMC7073502
OpenAlexW3010508594

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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.