Evidence map›Paper›PMID 21207215›Full record

ArticleInternational journal of hematology2011

Down-regulating the expression of IL-3Rβ interfered with the proliferation, not differentiation in NB4 cells.

Xin Li, Yong Wu, Yuanzhong Chen

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Article in International journal of hematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Xin LiFujian Institute of Hematology, Union Hospital Affiliated to Fujian Medical University, 29 Xinquan Road, Fuzhou 350001, Fujian, People's Republic of China.
Yong Wu
Yuanzhong Chen
Fujian Medical University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human IL-3 receptor is composed of both α and β subunits. In early studies, we showed that the level of IL-3Rβ expression was lower in patients with acute promyelocytic leukemia (APL) than healthy donors and patients in complete remission by real-time quantitative polymerase chain reaction (RT-qPCR). With the differentiation of cells, enhanced expression of IL-3Rβ was also observed in all-trans-retinoic acid (ATRA)-induced NB4 cells. To unravel the role of IL-3Rβ upregulation in NB4 cells induced with ATRA, we knocked down IL-3Rβ expression by RNA interference (RNAi). Knockdown of IL-3Rβ resulted in decreased proliferation in NB4 cells induced with or without ATRA, observed by cell growth curves, colony formation assays and cell cycle analysis. Surface expression of CD11b antigen and nitroblue tetrazolium (NBT) reduction assays were also carried out at different time points. However, no significant difference was observed between the experimental and control groups treated with ATRA. Other findings suggested that IL-3Rα was decreased in NB4-IL-3Rβ shRNA cells by western blot. Down-regulation of IL-3Rβ also caused a decrease in PML/RARα expression detected with RT-qPCR. Together, these results suggest that abnormalities of IL-3Rβ expression were observed in APL; knockdown of IL-3Rβ inhibited the proliferation of NB4 cells with or without ATRA, but no effect was detected in the cellular differentiation. When NB4 cells exposed to ATAR, the up-regulation of IL-3Rβ expression may contribute to the maintenance of proliferation rather than cell differentiation.

Indexed as

Cell ProliferationDown-RegulationAntineoplastic AgentsCell DifferentiationCytokine Receptor Common beta SubunitGene Expression Regulation, LeukemicGene Knockdown TechniquesHumansInterleukin-3 Receptor alpha SubunitLeukemia, Promyelocytic, AcuteTretinoinTumor Cells, CulturedAntineoplastic AgentsCytokine Receptor Common beta SubunitIL3RA protein, humanInterleukin-3 Receptor alpha SubunitTretinoin

Identifiers

PMID21207215
OpenAlexW2059373337

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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.