ZBTB7A, a miR-144-3p targeted gene, accelerates bladder cancer progression via downregulating HIC1 expression.

Bladder cancer HIC1 ZBTB7A miR-144-3p

Journal

Cancer cell international
ISSN: 1475-2867
Titre abrégé: Cancer Cell Int
Pays: England
ID NLM: 101139795

Informations de publication

Date de publication:
02 May 2022
Historique:
received: 19 11 2021
accepted: 18 04 2022
entrez: 3 5 2022
pubmed: 4 5 2022
medline: 4 5 2022
Statut: epublish

Résumé

Zinc finger and BTB domain-containing 7A (ZBTB7A) is a member of the POK family of transcription factors that plays an oncogenic or tumor-suppressive role in different cancers depending on the type and genetic context of cancer. However, the function and molecular mechanism of ZBTB7A in bladder cancer (BC) remain elusive. The role of ZBTB7A in bladder cancer was detected by colony formation, transwell, and tumor formation assays. The expression levels of ZBTB7A, HIC1, and miR-144-3p were analyzed by qRT-PCR and Western blot. Bioinformatics analysis and a dual-luciferase reporter assay were used to assess the effect of ZBTB7A on the promoter activity of HIC1. The present study revealed that knockdown of ZBTB7A suppressed BC cell growth and migration, as indicated by an approximately 50% reduction in the number of colonies and an approximately 70% reduction in the number of migrated cells. Loss of ZBTB7A inhibited tumor growth in vivo, resulting in a 75% decrease in tumor volume and an 80% decrease in tumor weight. Further mechanistic studies revealed that ZBTB7A bound to the hypermethylated in cancer 1 (HIC1) promoter and downregulated HIC1 expression, accelerating the malignant behavior of BC. Increased expression of ZBTB7A in BC tissues was negatively corrected with the expression of HIC1. Moreover, ZBTB7A was a target of miR-144-3p, which decreased ZBTB7A expression in BC. Our data demonstrate that ZBTB7A, a targeted gene of miR-144-3p, promoted tumorigenesis of BC through downregulating HIC1 expression.

Sections du résumé

BACKGROUND BACKGROUND
Zinc finger and BTB domain-containing 7A (ZBTB7A) is a member of the POK family of transcription factors that plays an oncogenic or tumor-suppressive role in different cancers depending on the type and genetic context of cancer. However, the function and molecular mechanism of ZBTB7A in bladder cancer (BC) remain elusive.
METHODS METHODS
The role of ZBTB7A in bladder cancer was detected by colony formation, transwell, and tumor formation assays. The expression levels of ZBTB7A, HIC1, and miR-144-3p were analyzed by qRT-PCR and Western blot. Bioinformatics analysis and a dual-luciferase reporter assay were used to assess the effect of ZBTB7A on the promoter activity of HIC1.
RESULTS RESULTS
The present study revealed that knockdown of ZBTB7A suppressed BC cell growth and migration, as indicated by an approximately 50% reduction in the number of colonies and an approximately 70% reduction in the number of migrated cells. Loss of ZBTB7A inhibited tumor growth in vivo, resulting in a 75% decrease in tumor volume and an 80% decrease in tumor weight. Further mechanistic studies revealed that ZBTB7A bound to the hypermethylated in cancer 1 (HIC1) promoter and downregulated HIC1 expression, accelerating the malignant behavior of BC. Increased expression of ZBTB7A in BC tissues was negatively corrected with the expression of HIC1. Moreover, ZBTB7A was a target of miR-144-3p, which decreased ZBTB7A expression in BC.
CONCLUSION CONCLUSIONS
Our data demonstrate that ZBTB7A, a targeted gene of miR-144-3p, promoted tumorigenesis of BC through downregulating HIC1 expression.

Identifiants

pubmed: 35501800
doi: 10.1186/s12935-022-02596-w
pii: 10.1186/s12935-022-02596-w
pmc: PMC9063087
doi:

Types de publication

Journal Article

Langues

eng

Pagination

179

Subventions

Organisme : National Natural Science Foundation of China
ID : 11872146

Informations de copyright

© 2022. The Author(s).

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Auteurs

Junqiang Liu (J)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Zhiyuan Chou (Z)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Chun Li (C)

Central Laboratory, Affiliated Zhongshan Hospital of Dalian University, Dalian, China.

Kai Huang (K)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Xuejian Wang (X)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Xiunan Li (X)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Chuanchun Han (C)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Abdullah Al-Danakh (A)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China.

Xiaodong Li (X)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China. xd_li201212@dmu.edu.cn.

Xishuang Song (X)

Department of Urology of First Affiliated Hospital, Institute of Cancer Stem Cell, Dalian Medical University, Dalian, China. song-xishuang@163.com.

Classifications MeSH