Evidence map›Paper›PMID 38530586›Full record

ArticleInternational journal of hematology2024

Rapamycin increases leukemia cell sensitivity to chemotherapy by regulating mTORC1 pathway-mediated apoptosis and autophagy.

Jing Xu, Siwen Zong, Tianle Sheng, Jifu Zheng, Qiong Wu, Qingming Wang, Aiping Tang, Yuan Song, Yan Fei, Zhenjiang Li

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2024. 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
1.9field-weighted citation impact, top 14% 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, 5 citations in OpenAlex.

  1. 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

10 authors at 1 institution in 1 country.

Jing XuDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.
Siwen ZongSecond Clinical Medical College, Nanchang University, Nanchang, 330006, China.
Tianle ShengDepartment of Clinical Laboratory, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Jifu ZhengDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.
Qiong WuDepartment of Clinical Laboratory, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
Qingming WangDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.
Aiping TangDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.
Yuan SongDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.
Yan FeiDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China.
Zhenjiang LiDepartment of Hematology, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang, 330006, China. lzjdgh@163.com.ORCID http://orcid.org/0000-0001-7559-637X
Nanchang University · CN

Funding

Jiangxi "5511" Science and Technology Innovation Talent Project 20171BCB18003the National Natural Science Foundation of China 82260037
6 · The paper itself

Abstract

This study investigated the effect of rapamycin alone and in combination with chemotherapy (doxorubicin and cytarabine) on AML. Human acute monocytic leukemia cell line SHI-1 and NPG AML model mice created by intravenous injection of SHI-1 cell were treated with rapamycin, chemotherapy, or rapamycin plus chemotherapy. Analysis by cell counting kit-8, western blot, flow cytometry, and immunohistochemistry was performed, and results suggested that both rapamycin and chemotherapy inhibited proliferation of SHI-1 cells both in vitro and in vivo, suppressed neoplasm growth in vivo, and promoted survival of NPG AML mice. The antitumor effect of rapamycin plus chemotherapy was better than that of rapamycin alone and chemotherapy alone. In addition, western blot results demonstrated that rapamycin inhibited the phosphorylation of mTOR downstream targets 4EBP1 and S6K1 in SHI-1 cells, and increased the pro-apoptosis-related protein Bax and autophagy-associated proteins Beclin-1, LC3B-II, and ATG5 while reducing the anti-apoptosis-related protein Bcl-2. In conclusion, the results of this study indicate that rapamycin acts synergistically with doxorubicin and cytarabine in AML treatment, and its underlying mechanism might be associated with mTORC1 pathway-mediated apoptosis and autophagy.

Indexed as

ApoptosisAutophagyDoxorubicinMechanistic Target of Rapamycin Complex 1Signal TransductionSirolimusAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorCell ProliferationCytarabineDrug SynergismHumansLeukemia, Myeloid, AcuteMiceXenograft Model Antitumor AssaysCytarabineDoxorubicinMechanistic Target of Rapamycin Complex 1Sirolimus4EBP1ApoptosisLeukemiamTORRapamycinS6K1

Identifiers

PMID38530586
OpenAlexW4393182587

What OpenQuestion holds

Textmetadata
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.