Evidence map›Paper›PMID 33663588›Full record

ArticleBiomarker research2021

Inhibition of BCL11B induces downregulation of PTK7 and results in growth retardation and apoptosis in T-cell acute lymphoblastic leukemia.

Kehan Li, Cunte Chen, Rili Gao, Xibao Yu, Youxue Huang, Zheng Chen, Zhuandi Liu, Shaohua Chen, Gengxin Luo, Xin Huang and 3 more

Open access · goldAbstract readLetter
In one paragraph

Article in Biomarker research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-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

18 citing papers in PubMed, 32 citations in OpenAlex.

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  14. Clinical Medicine Insights. Oncology · 2023
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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

13 authors at 5 institutions in 3 countries.

Kehan Li *Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Cunte Chen *Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Rili Gao *Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Xibao YuKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Youxue HuangKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Zheng ChenKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Zhuandi LiuKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Shaohua ChenKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China.
Gengxin LuoDepartment of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, 510632, P.R. China.
Xin HuangDepartment of Hematology, Guangdong General Hospital (Guangdong Academy of Medical Sciences), Guangzhou, 510080, P.R. China.
Grzegorz K PrzybylskiInstitute of Human Genetics, Polish Academy of Sciences, Strzeszyńska 32, 60-479, Poznań, Poland. grzegorz.przybylski@igcz.poznan.pl.
Yangqiu LiKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China. yangqiuli@hotmail.com.
Chengwu ZengKey Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, P.R. China. bio-zcw@163.com.ORCID http://orcid.org/0000-0002-1333-3918
Jinan University · CNFirst Affiliated Hospital of Jinan University · CNGuangdong General Hospital · CNInstitute of Human Genetics · PLMinistry of Education of the People's Republic of China · CN

Funding

International Science and Technology Cooperation Programme 2017YFE0131600Major Research Plan 81770158National Science Center (PL) DEC-2013/09/B/NZ1/01867Pearl River S and T Nova Program of Guangzhou 201906010002Polish National Centre for Research and Development WPC1/BCL/2019Science and Technology Planning Project of Guangdong Province 2020A0505100042
6 · The paper itself

Abstract

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive subtype of leukemia with poor prognosis, and biomarkers and novel therapeutic targets are urgently needed for this disease. Our previous studies have found that inhibition of the B-cell leukemia/lymphoma 11B (BCL11B) gene could significantly promote the apoptosis and growth retardation of T-ALL cells, but the molecular mechanism underlying this effect remains unclear. This study intends to investigate genes downstream of BCL11B and further explore its function in T-ALL cells. We found that PTK7 was a potential downstream target of BCL11B in T-ALL. Compared with the healthy individuals (HIs), PTK7 was overexpressed in T-ALL cells, and BCL11B expression was positively correlated with PTK7 expression. Importantly, BCL11B knockdown reduced PTK7 expression in T-ALL cells. Similar to the effects of BCL11B silencing, downregulation of PTK7 inhibited cell proliferation and induced apoptosis in Molt-4 cells via up-regulating the expression of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and p27. Altogether, our studies suggest that PTK7 is a potential downstream target of BCL11B, and downregulation of PTK7 expression via inhibition of the BCL11B pathway induces growth retardation and apoptosis in T-ALL cells.

Identifiers

PMID33663588
PMCPMC7934371
OpenAlexW3134574901

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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.