Evidence map›Paper›PMID 25534115›Full record

ArticleJournal of cellular and molecular medicine2015

ASPP2 enhances oxaliplatin (L-OHP)-induced colorectal cancer cell apoptosis in a p53-independent manner by inhibiting cell autophagy.

Ying Shi, Yue Han, Fang Xie, Anna Wang, Xiaokun Feng, Ning Li, Hongliang Guo, Dexi Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

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  11. Expression and significance of ASPP2 in squamous carcinoma of esophagus.The Kaohsiung journal of medical sciences · 2018
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  18. ΔN-ASPP2, a novel isoform of the ASPP2 tumor suppressor, promotes cellular survival.Biochemical and biophysical research communications · 2017
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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 5 institutions in 1 country.

Ying ShiBeijing Youan Hospital, Capital University of Medical Sciences, Beijing, China; Beijing Institute of Hepatology, Beijing, China.
Yue Han
Fang Xie
Anna Wang
Xiaokun Feng
Ning Li
Hongliang Guo
Dexi Chen
Beijing Institute of Neurosurgery · CNBeijing YouAn Hospital · CNShandong First Medical University · CNShandong Tumor Hospital · CNUniversity of Jinan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inactivation of p53-mediated cell death pathways is a central component of cancer progression. ASPP2 (apoptosis stimulated protein of p53-2) is a p53 binding protein that specially stimulates pro-apoptosis function of p53. Down-regulation of ASPP2 is observed in many human cancers and is associated with poor prognosis and metastasis. In this study, ASPP2 was found to enhance L-OHP-induced apoptosis in HCT116 p53(-/-) cells in a p53-independent manner. Such apoptosis-promoting effect of ASPP2 was achieved by inhibiting autophagy. Further experiments with ASPP2 RNA interference and autophagy inhibitor (3-methyladenine, 3-MA) confirmed that ASPP2 enhanced HCT116 p53(-/-) cell apoptosis via inhibiting the autophagy. The association of cell death and autophagy was also found in ASPP2(+/-) mice, where colon tissue with reduced ASPP2 expression displayed more autophagy and less cell death. Finally, colorectal tumours and their adjacent normal tissues from 20 colorectal cancer patients were used to examine ASPP2 expression, p53 expression and p53 mutation, to understand their relationships with the patients' outcome. Three site mutations were found in p53 transcripts from 16 of 20 patients. ASPP2 mRNA expressions were higher, and autophagy level was lower in the adjacent normal tissues, compared with the tumour tissues, which was independent of both p53 mutation and expression level. Taken together, ASPP2 increased tumour sensitivity to chemotherapy via inhibiting autophagy in a p53-independent manner, which was associated with the tumour formation, suggesting that both p53 inactivation and ASPP2 expression level were involved in the sensitivity of colorectal cancer to chemotherapy.

Indexed as

AdenineAnimalsAntineoplastic AgentsApoptosisApoptosis Regulatory ProteinsAutophagyCell Line, TumorColorectal NeoplasmsFemaleHCT116 CellsHumansMaleMiceMice, Inbred BALB CMice, TransgenicMiddle Aged3-methyladenineAdenineAntineoplastic AgentsApoptosis Regulatory ProteinsOrganoplatinum CompoundsOxaliplatinRNA, Small InterferingTP53BP2 protein, humanTumor Suppressor Protein p53apoptosisASPP2autophagycolorectal cancerp53

Identifiers

PMID25534115
PMCPMC4369811
OpenAlexW2022021283

What OpenQuestion holds

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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.