Evidence map›Paper›PMID 33931087›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

ZBTB28 induces autophagy by regulation of FIP200 and Bcl-XL facilitating cervical cancer cell apoptosis.

Li Li, Yijia Gong, Ke Xu, Weihong Chen, Jiuyi Xia, Zhaobo Cheng, Lili Li, Renjie Yu, Junhao Mu, Xin Le and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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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

14 authors at 2 institutions in 1 country.

Li Li *Department of Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yijia Gong *Department of Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ke Xu *Department of Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Weihong ChenChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Jiuyi XiaChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Zhaobo ChengChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Lili LiCancer Epigenetics Laboratory, Department of Clinical Oncology, State Key Laboratory of Translational Oncology, Sir YK Pao Center for Cancer and Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China.
Renjie YuChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Junhao MuChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Xin LeChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Qin XiangChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Weiyan PengChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China.
Junying TangDepartment of Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Tingxiu XiangChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Road, Chongqing, 400016, Yuzhong District, China. xiangtx@cqmu.edu.cn.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

National Natural Science Foundation of China #81372238, 81572769Natural Science Foundation of Chongqing 2020ZYO13799Natural Science Foundation of Chongqing cstc2020jcyj-bshX0026
6 · The paper itself

Abstract

backgroundAmong the common preventable cancers of women, cervical cancer has the highest morbidity. It is curable if detected at an early stage. However, reliable diagnostic and prognostic markers, which relate to physiologic and pathologic regulation of cervical cancer, are not available. In this study, one such potential marker, ZBTB28, was evaluated for its potential usefulness in cervical cancer assessment.

methodsPublic database analysis, reverse-transcription polymerase chain reaction (PCR), and methylation-specific PCR were employed to analyze ZBTB28 expression and promoter methylation. The importance of ZBTB28 in cervical cancer cells was assessed by cellular and molecular analysis in vitro and in vivo.

resultsThis study assessed the anti-tumor effects of the transcription factor, ZBTB28, which is often silenced in cervical cancer due to CpG methylation of its promoter. We found ZBTB28 to directly affect cervical cancer cell proliferation, apoptosis, autophagy, and tumorigenesis. Also, it increased cancer cell chemosensitivity to Paclitaxel, Cisplatin, and 5-fluorouracil. Ectopic ZBTB28 expression inhibited the growth of cervical cancer xenografts in nude mice. Furthermore, electron microscopy demonstrated ZBTB28 to induce autophagosomes in cervical cancer cells. ZBTB28 induced cellular autophagy by the degradation of Bcl-XL, reduction of the Bcl-XL-BECN1 complex, and by interaction with the autophagy-related gene FIP200. ZBTB28-induced autophagy of cervical cancer cells was shown to mediate cellular apoptosis through the regulation of FIP200.

conclusionThese findings identify ZBTB28 as a tumor suppressor gene that can induce autophagy-related apoptosis in cervical cancer cells. As such, ZBTB28 may be a target for the treatment of uterine-cervical carcinoma. Further, ZBTB28 promoter methylation analysis may offer a new objective strategy for cervical cancer screening.

Indexed as

Zinc FingersAnimalsApoptosisAutophagyAutophagy-Related Proteinsbcl-X ProteinCell Line, TumorFemaleGenes, Tumor SuppressorHEK293 CellsHeLa CellsHeterograftsHumansMiceMice, NudeTumor Suppressor ProteinsAutophagy-Related ProteinsBCL2L1 protein, humanbcl-X ProteinRB1CC1 protein, humanTumor Suppressor ProteinsApoptosisAutophagyBECN1Cervical cancerFIP200ZBTB28

Identifiers

PMID33931087
PMCPMC8086320
OpenAlexW3157476147

What OpenQuestion holds

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LicenceCC BY
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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.