Evidence map›Paper›PMID 26334958›Full record

ArticleOncotarget2015

TRIP-Br1 oncoprotein inhibits autophagy, apoptosis, and necroptosis under nutrient/serum-deprived condition.

Samil Jung, Chengping Li, Jingjing Duan, Soonduck Lee, Kyeri Kim, Yeonji Park, Young Yang, Keun-Il Kim, Jong-Seok Lim, Chung-Il Cheon and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  9. Targeting ferroptosis in breast cancer.Biomarker research · 2020
    Review
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  12. 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

12 authors at 1 institution in 1 country.

Samil JungDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Chengping LiDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Jingjing DuanDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Soonduck LeeDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Kyeri KimDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Yeonji ParkDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Young YangDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Keun-Il KimDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Jong-Seok LimDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Chung-Il CheonDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Young-Sook KangCollege of Pharmacy, Sookmyung Women's University, Seoul, 140-742, South Korea.
Myeong-Sok LeeDepartment of Life Systems, Sookmyung Women's University, Seoul, 140-742, South Korea.
Sookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TRIP-Br1 oncogenic protein has been shown to have multiple biological functions in cells. In this study, we demonstrate that TRIP-Br1 functions as an oncoprotein by inhibiting autophagy, apoptosis, and necroptosis of cancer cells and eventually helping them to survive under the nutrient/serum starved condition. TRIP-Br1 expression level was significantly increased in conditions with low levels of nutrients. Nutrient depleted conditions were induced by culturing cancer cells until they were overcrowded with high cell density or in media deprived of glucose, amino acids, or serum. Among them, serum starvation significantly enhanced the expression of TRIP-Br1 only in all tested breast cancer cell lines (MCF7, MDA-MB-231, T47D, MDA-MB-435, Hs578D, BT549, and MDA-MB-435) but not in the three normal cell lines (MCF10A, HfCH8, and NIH3T3). As compared with the control cells, the introduction of TRIP-Br1 silencing siRNA into MCF7 and MDA-MB-231 cells accelerated cell death by inducing apoptosis and necroptosis. In this process, TRIP-Br1 confers resistance to serum starvation-induced cell deaths by stabilizing the XIAP protein and inhibiting cellular ROS production. Moreover, our data also show that the intracellular increase of TRIP-Br1 protein resulting from serum starvation seems to occur in part through the blockage of PI3K/AKT signaling pathway.

Indexed as

ApoptosisAutophagyAmino AcidsAnimalsBreast NeoplasmsCell SurvivalCulture Media, Serum-FreeFemaleGene Expression Regulation, NeoplasticGlucoseHumansMCF-7 CellsMiceNecrosisNIH 3T3 CellsNuclear ProteinsAmino AcidsCulture Media, Serum-FreeGlucoseNuclear ProteinsPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSERTAD1 protein, humanTrans-ActivatorsTranscription FactorsXIAP protein, humanX-Linked Inhibitor of Apoptosis Proteinapoptosisautophagynecroptosisnutrient/serum starvationTRIP-Br1

Identifiers

PMID26334958
PMCPMC4745711
OpenAlexW2179886742

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.