Evidence map›Paper›PMID 24104394›Full record

ArticleLeukemia2014

MicroRNA187 overexpression is related to tumor progression and determines sensitivity to bortezomib in peripheral T-cell lymphoma.

Z-X Yan, L-L Wu, K Xue, Q-L Zhang, Y Guo, M Romero, C Leboeuf, A Janin, S-J Chen, L Wang and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2014. 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
4.0field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
  2. Review
  3. Exploration of the miR-187-3p/CNR2 pathway in modulating osteoblast differentiation and treating postmenopausal osteoporosis through mechanical stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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  16. Development and Significance of Mouse Models in Lymphoma Research.Current hematologic malignancy reports · 2019
    Review
  17. miR-217-casein kinase-2 cross talk regulates ERK activation in ganglioglioma.Journal of molecular medicine (Berlin, Germany) · 2017
    Article
  18. T-cell lymphomas, a challenging disease: types, treatments, and future.International journal of clinical oncology · 2017
    Review
  19. Article
  20. 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

11 authors at 4 institutions in 2 countries.

Z-X Yan1] State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China [2] Pôle de Recherches Sino-Français en Science du Vivant et Génomique, Laboratory of Molecular Pathology, Shanghai, China.
L-L WuDepartment of Pathology, Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
K XueDepartment of Medical Oncology, Shanghai Cancer Center, Fudan University, Shanghai, China.
Q-L ZhangDepartment of Medical Oncology, Shanghai Cancer Center, Fudan University, Shanghai, China.
Y GuoDepartment of Medical Oncology, Shanghai Cancer Center, Fudan University, Shanghai, China.
M RomeroUMR-S728, Laboratoire de Pathologie, Université Paris Diderot, Sorbonne Paris Cité, Paris, France.
C LeboeufUMR-S728, Laboratoire de Pathologie, Université Paris Diderot, Sorbonne Paris Cité, Paris, France.
A JaninUMR-S728, Laboratoire de Pathologie, Université Paris Diderot, Sorbonne Paris Cité, Paris, France.
S-J Chen1] State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China [2] Pôle de Recherches Sino-Français en Science du Vivant et Génomique, Laboratory of Molecular Pathology, Shanghai, China.
L Wang1] State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China [2] Pôle de Recherches Sino-Français en Science du Vivant et Génomique, Laboratory of Molecular Pathology, Shanghai, China.
W-L Zhao1] State Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Shanghai Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China [2] Pôle de Recherches Sino-Français en Science du Vivant et Génomique, Laboratory of Molecular Pathology, Shanghai, China.
Délégation Paris 7 · FRFudan University Shanghai Cancer Center · CNShanghai Institute of Hematology · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRs) are involved in tumorigenesis by regulating tumor suppressor genes and/or oncogenes. MiR187 was overexpressed in peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) and associated with high Ki67 expression, elevated lactate dehydrogenase, advanced International Prognostic Index and poor prognosis of patients. In vitro, ectopic expression of miR187 in T-lymphoma cell lines accelerated tumor cell proliferation, whereas treatment with miR187 inhibitor reduced cell growth. MiR187 downregulated tumor suppressor gene disabled homolog-2 (Dab2), decreased the interaction of Dab2 with adapter protein Grb2, resulting in Ras activation, phosphorylation/activation of extracellular signal-regulated kinase (ERK) and AKT, and subsequent stabilization of MYC oncoprotein. MiR187-overexpressing cells were resistant to chemotherapeutic agents like doxorubicin, cyclophosphamide, cisplatin and gemcitabine, but sensitive to the proteasome inhibitor bortezomib. Bortezomib inhibited T-lymphoma cell proliferation by downregulating miR187, dephosphorylating ERK and AKT and degrading MYC. In a murine xenograft model established with subcutaneous injection of Jurkat cells, bortezomib particularly retarded the growth of miR187-overexpressing tumors, consistent with the downregulation of miR187, Ki67 and MYC expression. Collectively, these findings indicated that miR187 was related to tumor progression in PTCL-NOS through modulating Ras-mediated ERK/AKT/MYC axis. Although potentially oncogenic, miR187 indicated the sensitivity of T-lymphoma cells to bortezomib. Cooperatively targeting ERK and AKT could be a promising clinical strategy in treating MYC-driven lymphoid malignancies.

Indexed as

AnimalsAntineoplastic AgentsBoronic AcidsBortezomibCell Line, TumorCell ProliferationDisease ProgressionExtracellular Signal-Regulated MAP KinasesHumansLymphoma, T-Cell, PeripheralMiceMicroRNAsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycPyrazinesAntineoplastic AgentsBoronic AcidsBortezomibExtracellular Signal-Regulated MAP KinasesMicroRNAsMIRN187 microRNA, humanMYC protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mycPyrazines

Identifiers

PMID24104394
OpenAlexW2030506447

What OpenQuestion holds

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Registered trials

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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.