Evidence map›Paper›PMID 40825899›Full record

ArticleAnnals of hematology2025

Sirolimus modulates the erythroid differentiation of K562 cells by upregulating SHP1.

Yuan Yang, Zengwei Tang, Qinglin Hu, Chen Yang, Miao Chen, Hongmei Jing, Bing Han

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Thoughts on the application of sirolimus.Annals of hematology · 2025
    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

7 authors.

Yuan YangDepartment of Hematology, Lymphoma Research Center, Peking University Third Hospital, Beijing, 100191, China.
Zengwei TangKey Laboratory of Cancer and Microbiome, State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID http://orcid.org/0000-0002-2711-795X
Qinglin HuDepartment of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100730, China.
Chen YangDepartment of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100730, China.
Miao ChenDepartment of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100730, China.
Hongmei JingDepartment of Hematology, Lymphoma Research Center, Peking University Third Hospital, Beijing, 100191, China.
Bing HanDepartment of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100730, China. hanbing_li2022@163.com.

Funding

Beijing Natural Science Foundation 7232109CAMS Innovation Fund for Medical Sciences CIFMS 2023-12M-C&T-B-013National High Level Hospital Clinical Research Funding 2022-PUMCH-C-026National Natural Science Foundation 82370121
6 · The paper itself

Abstract

Sirolimus is an effective treatment for acquired pure red cell aplasia (aPRCA), but the detail mechanism of sirolimus on red cell differentiation is incompletely understood. The aim of the study was to investigate whether sirolimus can induce the erythroid differentiation of K562 cells and investigate the potential regulation mechanism. Benzidine staining and flow cytometry were performed to determine the benzidine-/CD71-positive K562 cells with or without sirolimus treatment. The expression level of α-/ γ-globin in each group was determined by real-time qPCR, respectively. siRNA-targeted assays were performed to investigate the role of protein tyrosine phosphatase 1 (SHP1) in sirolimus-induced erythroid differentiation of K562 cells. The proportion of benzidine-staining/CD71-positive cells, and α- / γ-globin mRNA expression were increased in K562 cells treated with sirolimus. Sirolimus markedly inhibited mTOR and p-mTOR expression while upregulated SHP1 expression in K562 cells. Knockdown of SHP1 decrease α-/γ-globin mRNA level, CD71 protein expression levels and the proportion of benzidine-positive cells in the K562 cells. Additionally, knockdown of SHP1 can reverse the sirolimus-induced erythroid differentiation of K562 cells. Sirolimus treatment can promote the erythroid differentiation of K562 cells via upregulating of SHP1.

Indexed as

Cell DifferentiationErythroid CellsProtein Tyrosine Phosphatase, Non-Receptor Type 6SirolimusUp-Regulationgamma-GlobinsHumansK562 CellsTOR Serine-Threonine Kinasesgamma-GlobinsMTOR protein, humanProtein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, humanSirolimusTOR Serine-Threonine KinasesErythroid differentiationK562 cellSHP1Sirolimus

Identifiers

PMID40825899
PMCPMC12432031

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.