Evidence map›Paper›PMID 25501832›Full record

ArticleCell death & disease2014

BMPR2 inhibition induced apoptosis and autophagy via destabilization of XIAP in human chondrosarcoma cells.

G Jiao, W Guo, T Ren, Q Lu, Y Sun, W Liang, C Ren, K Yang, K Sun

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

G JiaoMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
W GuoMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
T RenMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
Q LuMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
Y SunMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
W LiangMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
C RenMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
K YangMusculoskeletal Tumor Center, Peking University People's Hospital, Beijing 100044, People's Republic of China.
K SunDepartment of Pathology, Peking University People's Hospital, Beijing 100044, People's Republic of China.
Peking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone morphogenetic proteins (BMPs) are multifunctional proteins, and their receptors (BMPRs) have crucial roles in the process of signaling. However, their function in cancer is somewhat inconsistent. It has been demonstrated that more prevalent expression of bone morphogenetic protein receptor 2 (BMPR2) has been detected in dedifferentiated chondrosarcomas than conventional chondrosarcomas. Here, we find that BMPR2 inhibition induces apoptosis and autophagy of chondrosarcoma. We found that BMPR2 expression was correlated with the clinicopathological features of chondrosarcomas, and could predict the treatment outcome. Knockdown of BMPR2 by small interfering RNA results in growth inhibition in chondrosarcoma cells. Silencing BMPR2 promoted G2/M cell cycle arrest, induced chondrosarcoma cell apoptosis through caspase-3-dependent pathway via repression of X-linked inhibitor of apoptosis protein (XIAP) and induced autophagy of chondrosarcoma cells via XIAP-Mdm2-p53 pathway. Inhibition of autophagy induced by BMPR2 small interfering RNA (siBMPR2) sensitized chondrosarcoma cells to siBMPR2-induced apoptotic cell death, suggesting that autophagy has a protective role for chondrosarcoma cells in context of siBMPR2-induced apoptotic cell death. In vivo tumorigenicity assay in mice indicated that inhibition of BMPR2 reduced tumor growth. Taken together, our results suggest that BMPR2 has a significant role in the tumorigenesis of chondrosarcoma, and could be an important prognostic marker for chondrosarcoma. BMPR2 inhibition could eventually provide a promising therapy for chondrosarcoma treatment.

Indexed as

ApoptosisAutophagyAnimalsBone Morphogenetic Protein Receptors, Type IICaspase 3Cell Line, TumorChondrosarcomaFemaleG2 Phase Cell Cycle CheckpointsHumansMiceMice, Inbred BALB CNeoplasms, Connective TissueProtein StabilityProto-Oncogene Proteins c-mdm2RNA InterferenceBone Morphogenetic Protein Receptors, Type IICaspase 3MDM2 protein, humanProto-Oncogene Proteins c-mdm2RNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53XIAP protein, humanX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID25501832
PMCPMC4649848
OpenAlexW2068626551

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.