Evidence map›Paper›PMID 29651698›Full record

ArticleJournal of natural medicines2018

Mitogenic activity of Artocarpus lingnanensis lectin and its apoptosis induction in Jurkat T cells.

Linjie Zeng, Lu Li, Qiyan Zeng, Yong Deng, Lijun Yin, Liejun Liao

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of natural medicines, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Frontiers in immunology · 2025
    Article
  2. Article
  3. 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

6 authors at 2 institutions in 1 country.

Linjie ZengDepartment of Orthopaedics, Chinese and Western, Orthopaedics Hospital of Guigang, Guigang, Guangxi, 537100, People's Republic of China.
Lu LiDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Qiyan ZengDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China. zengnn6@hotmail.com.
Yong DengDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Lijun YinDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Liejun LiaoDepartment of Biochemistry and Molecular Biology, Guangxi Medical University, 22 Shuangyong Road, Nanning, Guangxi, 530021, People's Republic of China.
Guangxi Medical University · CNGuigang Orthopedic Hospital of Integrated Traditional Chinese and Western Medicine · CN

Funding

Guangxi Natural Science Foundation Grant No. 0832130National Natural Science Foundation of China No.81160366
6 · The paper itself

Abstract

Lectins are a class of carbohydrate-binding proteins or glycoproteins and used in the purification and characterization of glycoproteins according to their specificity to carbohydrates. In the present study, the mitogenic activity of Artocarpus lingnanensis lectin (ALL) and its apoptosis induction in Jurkat T cells were explored. MTT assay revealed strong mitogenic potential of ALL. Meanwhile, the anti-cancer activity of ALL was also explored using the human leukemic Jurkat T cell line. ALL exhibited strong binding affinity (97%) to the cell membrane, which could be effectively inhibited by N-acetyl-D-galactosaminide (NAD). ALL induced time- and dose-dependent growth inhibition in Jurkat T cells. ALL could induce morphologic change and increase the hypodiploid cell population with the decreased population of S and G2/M phases. The induction of phosphatidylserine externalization and PARP cleavage further confirmed its apoptosis-inducing activity due to the activation of caspase-8 and -9. The inhibition of caspase-9 but not caspase-8 could rescue ALL-induced apoptotic cells. Further studies showed that ALL enhanced the cleavage of Bid, the release of cytochrome C, the depolarization of mitochondria and the activation of caspase-3. ALL downregulated the expression of Bcl-xl and Bcl-2 without impact on Bax and Bad. In addition, the activation of p38/JNK MAPK signaling pathways was observed to be a requisite for ALL apoptotic activity. In contrast, ALL could not induce apoptosis of normal T cells. These findings present the differential effect of ALL on Jurkat and normal T lymphocytes, suggesting its therapeutic value in leukemia.

Indexed as

AnimalsApoptosisArtocarpusCell ProliferationGlycoproteinsHumansJurkat CellsLectinsMiceMice, Inbred BALB CSignal TransductionGlycoproteinsLectinsApoptosisGlycoproteinLectinLeukemiaMitogenic activity

Identifiers

PMID29651698
OpenAlexW2798045065

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.