Evidence map›Paper›PMID 29445224›Full record

ArticleCell death & disease2018

Lup-20(29)-en-3β,28-di-yl-nitrooxy acetate affects MCF-7 proliferation through the crosstalk between apoptosis and autophagy in mitochondria.

Xiaoning Yan, Lei Yang, Gaili Feng, Zhuli Yu, Minjie Xiao, Weibin Cai, Yanmei Xing, Shasha Bai, Junqia Guo, Zhiyu Wang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.9field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
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  3. Frontiers in pharmacology · 2024
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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

12 authors at 2 institutions in 1 country.

Xiaoning YanInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Lei YangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Gaili FengSchool of Chinese Meteria Medica, Guangzhou University of Chinese Medicine, 510006, Guangzhou, China.
Zhuli YuInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Minjie XiaoSchool of Chinese Meteria Medica, Guangzhou University of Chinese Medicine, 510006, Guangzhou, China.
Weibin CaiInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Yanmei XingInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Shasha BaiInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Junqia GuoInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China.
Zhiyu WangGuangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, 510006, Guangzhou, China.
Tao WangSchool of Chinese Meteria Medica, Guangzhou University of Chinese Medicine, 510006, Guangzhou, China. wangtao@gzucm.edu.cn.
Rong ZhangInstitute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 510405, Guangzhou, China. zhangrong@gzucm.edu.cn.
Guangzhou University of Chinese Medicine · CNShanxi University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Betulin (BT), a pentacyclic lupine-type triterpenoid natural product, possesses antitumor activity in various types of cancers. However, its clinical development was discouraged due to its low biological activities and poor solubility. We prepared lup-20(29)-en-3β,28-di-yl-nitrooxy acetate (NBT), a derivative of BT, that was chemically modified at position 3 of ring A and C-28 by introducing a NO-releasing moiety. This study mainly explored the mechanism of NBT in treating breast cancer through the crosstalk between apoptosis and autophagy in mitochondria. NBT possessed a potent antiproliferative activity in MCF-7 cells both in vitro and in vivo. Mechanically, NBT affected cell death through the mitochondrial apoptosis pathway and autophagy. NBT induced cell cycle arrest in the G

Indexed as

Gene Expression Regulation, NeoplasticAnimalsAntineoplastic Agents, PhytogenicApoptosisAutophagybcl-2-Associated X ProteinBetulinic AcidBreast NeoplasmsCaspase 9Cell ProliferationChloroquineCyclin D1Cytochromes cDrug CombinationsFemaleFluorouracilAntineoplastic Agents, PhytogenicBAX protein, humanbcl-2-Associated X ProteinBCL2 protein, humanbetulinBetulinic AcidCASP9 protein, humanCaspase 9CCND1 protein, humanChloroquineCyclin D1Cytochromes cDrug CombinationsFluorouracilPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Triterpenes

Identifiers

PMID29445224
PMCPMC5833777
OpenAlexW2791051388

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.