Evidence map›Paper›PMID 24626183›Full record

ArticleCell cycle (Georgetown, Tex.)2014

RASSF6 promotes p21(Cip1/Waf1)-dependent cell cycle arrest and apoptosis through activation of the JNK/SAPK pathway in clear cell renal cell carcinoma.

Ying-Ying Liang, Li-Sheng Zheng, Yuan-Zhong Wu, Li-Xia Peng, Yun Cao, Xue Cao, Ping Xie, Bi-Jun Huang, Chao-Nan Qian

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Tumor suppressor C-RASSF proteins.Cellular and molecular life sciences : CMLS · 2018
    Review
  6. Article
  7. Article
  8. Article
  9. Ras signaling through RASSF proteins.Seminars in cell & developmental biology · 2016
    Review
  10. Review
  11. Article
  12. Article
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

9 authors at 2 institutions in 1 country.

Ying-Ying LiangState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Li-Sheng ZhengState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Yuan-Zhong WuState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Li-Xia PengState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Yun CaoDepartment of Pathology; Sun Yat-sen University Cancer Center; Guangzhou, China.
Xue CaoState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Ping XieState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Bi-Jun HuangState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Chao-Nan QianState Key Laboratory of Oncology in South China and Collaborative Innovation Center of Cancer Medicine; Sun Yat-sen University Cancer Center; Guangzhou, China.
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clear cell renal cell carcinoma (ccRCC) is a highly aggressive and common pathological subtype of renal cancer. This cancer is characterized by biallelic inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene, which leads to the accumulation of hypoxia-inducible factors (HIFs). Although therapies targeted at HIFs can significantly improve survival, nearly all patients with advanced ccRCC eventually succumb to the disease. Thus, additional oncogenic events are thought to be involved in the development of ccRCC tumors. In this study, we investigated the role of RASSF6 in ccRCC. Downregulation of RASSF6 was commonly observed in primary tumors relative to matched adjacent normal tissues. Moreover, functional studies established that ectopic re-expression of RASSF6 in ccRCC cells inhibited cell proliferation, clonogenicity, and tumor growth in mice, whereas silencing of RASSF6 dramatically enhanced cell proliferation in vitro and in vivo. Mechanistic investigation suggested that RASSF6 triggers p21(Cip1/Waf1) accumulation to induce G 1 cell cycle arrest and promote apoptosis upon exposure to pro-apoptotic agents, and both of these mechanisms appear to be mediated by activated JNK signaling. Together, these findings suggest that RASSF6 may play a tumor suppressor role in the progression of ccRCC.

Indexed as

ApoptosisG1 Phase Cell Cycle CheckpointsAnimalsApoptosis Regulatory ProteinsCarcinoma, Renal CellCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21HumansJNK Mitogen-Activated Protein KinasesKidney NeoplasmsMAP Kinase Signaling SystemMiceMice, NudeMonomeric GTP-Binding ProteinsApoptosis Regulatory ProteinsCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p21JNK Mitogen-Activated Protein KinasesMonomeric GTP-Binding ProteinsRASSF6 protein, humanapoptosisccRCCcell cycleJNK signalingp21Cip1/Waf1RASSF6

Identifiers

PMID24626183
PMCPMC4050141
OpenAlexW1973332845

What OpenQuestion holds

Textmetadata
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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.