Evidence map›Paper›PMID 30029665›Full record

ArticleJournal of translational medicine2018

Resibufogenin suppresses colorectal cancer growth and metastasis through RIP3-mediated necroptosis.

Qinrui Han, Ye Ma, Hao Wang, Yu Dai, Chunhui Chen, Yawei Liu, Linlin Jing, Xuegang Sun

Abstract read
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

82 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Resibufogenin protects against atherosclerosis in ApoEJournal of advanced research · 2026
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22 more citing papers are in PubMed but not listed here.

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.

Qinrui HanLaboratory of Molecular Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Ye MaLaboratory of Molecular Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Hao WangLaboratory of Molecular Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yu DaiLaboratory of Molecular Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Chunhui ChenLaboratory of Molecular Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China.
Yawei LiuThe Laboratory for Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Linlin JingTCM Integrated Hospital of Southern Medical University, Guangzhou, China.
Xuegang SunLaboratory of Molecular Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, Guangdong, China. sxg_smu@126.com.

Funding

National Natural Science Foundation of China 81472315National Natural Science Foundation of China 81573848National Natural Science Foundation of China 81774172Natural Science Foundation of Guangdong Province 2014A030313323
6 · The paper itself

Abstract

backgroundNecroptotic susceptibility is probably an intrinsic weakness of cancer. Here, we report that resibufogenin, a member of bufadienolide family, suppresses the growth and metastasis of colorectal cancer (CRC) through induction of necroptosis in vivo.

methodsSW480 cells with stably expressing enhanced green fluorescence protein were xenografted to BALB/c-nu mice to observe the growth of tumors. Liver metastasis was observed by injection of MC38 cells beneath the splenic capsule of mice. Protein expression was determined by immunohistochemistry, immunofluorescence and western blot.

resultsConsolidated in vitro results indicate that resibufogenin has anti-proliferative activity on CRC cells. PI staining and transmission electron microscope imaging suggest that the cell death induced by resibufogenin are mainly through necrosis, which is further confirmed by the ineffectiveness of z-VAD, a pan-caspase general inhibitor. In particular, resibufogenin induced necrosis is substantially abrogated in receptor-interacting protein kinase 3 (RIPK3) knockout mouse embryo fibroblasts. The RIP3-dependent necrosis has been classified as necroptosis. Resibufogenin triggeres necroptosis through upregulating RIP3 and phosphorylating mixed lineage kinase domain-like protein at Ser358. Resibufogenin also activates the expression of PYGL, GLUD1 and GLUL in a RIP3-dependent manner. Resibufogenin exerts cytotoxic effect by inducing reactive oxygen species accumulation which can be neutralized by N-acetylcysteine. Remarkably, resibufogenin significantly suppresses liver-metastasis from spleen implantation. The anti-neoplastic effect of this compound can be abrogated by RIP3 knockdown.

conclusionResibufogenin suppresses growth and metastasis of CRC through RIP3-mediated necroptosis.

Indexed as

AnimalsApoptosisBufanolidesCell Line, TumorCell ProliferationColorectal NeoplasmsHumansMiceNecrosisNeoplasm MetastasisReceptor-Interacting Protein Serine-Threonine KinasesBufanolidesbufogeninReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanRipk3 protein, mouseColorectal cancerMetastasisNecroptosisReceptor-interacting protein kinase 3Resibufogenin

Identifiers

PMID30029665
PMCPMC6053767

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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.