Evidence map›Paper›PMID 32242118›Full record

ArticleActa pharmacologica Sinica2020

RIP1 promotes proliferation through G2/M checkpoint progression and mediates cisplatin-induced apoptosis and necroptosis in human ovarian cancer cells.

Xue-Lian Zheng, Jiao-Jiao Yang, Yan-Yun Wang, Qin Li, Ya-Ping Song, Min Su, Jin-Ke Li, Lin Zhang, Zhi-Ping Li, Bin Zhou and 1 more

Abstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Establishment of a Prognostic Necroptosis-Related lncRNA Signature in Ovarian Cancer.Combinatorial chemistry & high throughput screening · 2026
    Article
  4. Therapeutic Effects ofPediatric discovery · 2025
    Article
  5. Targeting RIPK1 to modulate cell death and tumour microenvironment in cancer therapy.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  6. Article
  7. 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

11 authors.

Xue-Lian ZhengLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Jiao-Jiao YangDepartment of Abdominal Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yan-Yun WangLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Qin LiLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Ya-Ping SongLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Min SuLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Jin-Ke LiLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Lin ZhangLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China.
Zhi-Ping LiDepartment of Abdominal Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, 610041, China.
Bin ZhouLaboratory of Molecular and Translational Medicine, Center for Translational Medicine, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University) of Ministry of Education, Department of Obstetrics and Gynecology, West China Second University Hospital, Sichuan University, Chengdu, 610041, China. zb630@163.com.
Yong LinMolecular Biology and Lung Cancer Program, Lovelace Respiratory Research Institute, 2425 Ridgecrest Drive, SE, Albuquerque, NM, 87108, USA. ylin@lrri.org.

Funding

Targeting RIP3-mediated Necroptosis for ChemosensitizationR21CA193633 · NCI · LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE · PI LIN, YONG · 2016 to 2017
$515k
NCI NIH HHS R21 CA193633
6 · The paper itself

Abstract

Receptor-interacting protein 1 (RIP1, also known as RIPK1) is not only a tumor-promoting factor in several cancers but also mediates either apoptosis or necroptosis in certain circumstances. In this study we investigated what role RIP1 plays in human ovarian cancer cells. We showed that knockout (KO) of RIP1 substantially suppressed cell proliferation, accompanied by the G2/M checkpoint arrest in two human ovarian cancer cell lines SKOV3 and A2780. On the other hand, RIP1 KO remarkably attenuated cisplatin-induced cytotoxicity, which was associated with reduction of the apoptosis markers PARP cleavage and the necroptosis marker phospho-MLKL. We found that RIP1 KO suppressed cisplatin-induced ROS accumulation in both SKOV3 and A2780 cells. ROS scavenger BHA, apoptosis inhibitor Z-VAD or necroptosis inhibitor NSA could effectively suppress cisplatin's cytotoxicity in the control cells, suggesting that ROS-mediated apoptosis and necroptosis were involved in cisplatin-induced cell death. In addition, blocking necroptosis with MLKL siRNA effectively attenuated cisplatin-induced cytotoxicity. In human ovarian cancer A2780 cell line xenograft nude mice, RIP1 KO not only significantly suppressed the tumor growth but also greatly attenuated cisplatin's anticancer activity. Our results demonstrate a dual role of RIP1 in human ovarian cancer: it acts as either a tumor-promoting factor to promote cancer cell proliferation or a tumor-suppressing factor to facilitate anticancer effects of chemotherapeutics such as cisplatin.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCell Line, TumorCell ProliferationCisplatinFemaleG2 Phase Cell Cycle CheckpointsGene Knockout TechniquesHumansMice, Inbred BALB CMice, NudeNecroptosisOvarian NeoplasmsPaclitaxelReactive Oxygen SpeciesAntineoplastic AgentsCisplatinPaclitaxelReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanapoptosisBHAcisplatinnecroptosisNSAovarian cancerproliferationRIP1RIPK1ROStaxolZ-VAD

Identifiers

PMID32242118
PMCPMC7608477

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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.