Evidence map›Paper›PMID 31322275›Full record

ArticleOncology reports2019

AML‑derived mesenchymal stem cells upregulate CTGF expression through the BMP pathway and induce K562‑ADM fusiform transformation and chemoresistance.

Haiying Li, Juan Li, Juan Cheng, Xuan Chen, Lanxia Zhou, Zhao Li

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The CCN axis in cancer development and progression.Journal of cell communication and signaling · 2021
    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

6 authors at 2 institutions in 1 country.

Haiying LiDepartment of Central Laboratory, The First Medical College of Lanzhou University, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Juan LiDepartment of Central Laboratory, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Juan ChengDepartment of Hematology, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Xuan ChenDepartment of Central Laboratory, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Lanxia ZhouDepartment of Central Laboratory, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Zhao LiDepartment of Central Laboratory, The First Hospital of Lanzhou University, Lanzhou University, Lanzhou, Gansu 730000, P.R. China.
Lanzhou University · CNFirst Hospital of Lanzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow‑derived mesenchymal stem cells (MSCs), are the basic cellular components that make up the bone marrow microenvironment (BMM). In acute myeloid leukemia (AML), the morphology and function of MSCs changes in accordance with the transformation of the BMM. Moreover, the transformation of MSCs into osteoblasts is determined through the bone morphogenetic protein (BMP) pathway, ultimately leading to an altered expression of the downstream adhesion molecule, connective tissue growth factor (CTGF). In this study, we aimed to explore the interaction of possible pathways in AML‑derived mesenchymal stem cells (AML‑MSCs) co‑cultured with the K562 and K562‑ADM cell lines. AML‑MSCs were co‑cultured with K562/K562‑ADM cells, and the interactions between the cells were verified by morphological detection, peroxidase staining (POX), reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and fluorescence in situ hybridization (FISH). The proliferation of K562/K562‑ADM cells under co‑culture conditions was detected by flow cytometry. The expression levels of BMP4 and CTGF were examined by RT‑qPCR and western blot (WB) analysis. The detection of interleukin (IL)‑6 and IL‑32 was also determined by enzyme linked immunosorbent assay (ELISA). In the co‑culture system, the K562‑ADM cells underwent fusiform transformation. The occurrence of this transformation was associated with an increased expression of CTGF due to the dysregulation of the BMP pathway. The AML‑MSCs promoted the proliferation of the K562‑ADM cell, but inhibited that of the K562 cells. These findings were confirmed by changes in the expression of the soluble cytokines, IL‑6 and IL‑32. On the whole, the findings of this study demonstrate that AML‑MSCs regulate the expression of CTGF through the BMP pathway. In addition, they affect cytokine production, induce spindle‑shaped transformation, and increase drug resistance in the K562‑ADM cells. Thus, the morphological transformation through the BMP pathway provides us with a novel target with which to circumvent tumor occurrence, development, drug resistance, invasion and metastasis.

Indexed as

Drug Resistance, NeoplasmAdolescentAdultAgedAged, 80 and overApoptosisBone Morphogenetic Protein 4Cell CycleCell DifferentiationCell ProliferationCells, CulturedCell Transformation, NeoplasticChildConnective Tissue Growth FactorDoxorubicinFemaleBMP4 protein, humanBone Morphogenetic Protein 4CCN2 protein, humanConnective Tissue Growth FactorDoxorubicin

Identifiers

PMID31322275
PMCPMC6667869
OpenAlexW2959033869

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.