Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis

Abstract Colorectal cancer (CRC) is a prevalent malignant tumor of the digestive tract. Circular RNAs may play important roles in the progression of CRC. In this study, we investigated the roles and mechanisms of action of circ‐MALAT1 in CRC. Gene expression and protein abundance were determined usi...

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Main Authors: Feng‐Shuai Yang, Shuang‐Xi Gong, Dong‐Da Qiu
Format: Article
Language:English
Published: Wiley 2023-09-01
Series:Kaohsiung Journal of Medical Sciences
Subjects:
Online Access:https://doi.org/10.1002/kjm2.12698
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author Feng‐Shuai Yang
Shuang‐Xi Gong
Dong‐Da Qiu
author_facet Feng‐Shuai Yang
Shuang‐Xi Gong
Dong‐Da Qiu
author_sort Feng‐Shuai Yang
collection DOAJ
description Abstract Colorectal cancer (CRC) is a prevalent malignant tumor of the digestive tract. Circular RNAs may play important roles in the progression of CRC. In this study, we investigated the roles and mechanisms of action of circ‐MALAT1 in CRC. Gene expression and protein abundance were determined using qRT‐PCR and western blot, respectively. Cell proliferation and migration were assessed by MTT, clone formation, and wound‐healing assays. The interactions among the long non‐coding RNA metastasis‐associated lung adenocarcinoma transcript 1 (circ‐MALAT1), miR‐506‐3p, and lysine acetyltransferase 6B (KAT6B) were predicted using the StarBase software and confirmed by the luciferase activity assay. Circ‐MALAT1 and KAT6B were upregulated, while miR‐506‐3p was downregulated in CRC cells. We validated that knocking down of circ‐MALAT1 suppressed proliferation, migration, and epithelial–mesenchymal transition (EMT) of CRC cells, and these effects were abolished by miR‐506‐3p downregulation or KAT6B sufficiency. Our study suggests that circ‐MALAT1 could sponge miR‐506‐3p to regulate the expression of KAT6B. Moreover, KAT6B sufficiency could neutralize miR‐506‐3p‐dependent growth arrest, migration, and EMT. Circ‐MALAT1 promotes cell proliferation, migration, and EMT of CRC cells via the miR‐506‐3p/KAT6B axis, thereby acting as a novel potential therapeutic target for the treatment of colorectal cancer.
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spelling doaj.art-23af51b68ccb45caac8a18200153b2f22023-09-12T13:06:57ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502023-09-0139986287210.1002/kjm2.12698Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axisFeng‐Shuai Yang0Shuang‐Xi Gong1Dong‐Da Qiu2Department of Gastrointestinal Surgery The First Hospital of Changsha Changsha Hunan Province People's Republic of ChinaDepartment of Gastrointestinal Surgery The First Hospital of Changsha Changsha Hunan Province People's Republic of ChinaDepartment of Gastrointestinal Surgery The First Hospital of Changsha Changsha Hunan Province People's Republic of ChinaAbstract Colorectal cancer (CRC) is a prevalent malignant tumor of the digestive tract. Circular RNAs may play important roles in the progression of CRC. In this study, we investigated the roles and mechanisms of action of circ‐MALAT1 in CRC. Gene expression and protein abundance were determined using qRT‐PCR and western blot, respectively. Cell proliferation and migration were assessed by MTT, clone formation, and wound‐healing assays. The interactions among the long non‐coding RNA metastasis‐associated lung adenocarcinoma transcript 1 (circ‐MALAT1), miR‐506‐3p, and lysine acetyltransferase 6B (KAT6B) were predicted using the StarBase software and confirmed by the luciferase activity assay. Circ‐MALAT1 and KAT6B were upregulated, while miR‐506‐3p was downregulated in CRC cells. We validated that knocking down of circ‐MALAT1 suppressed proliferation, migration, and epithelial–mesenchymal transition (EMT) of CRC cells, and these effects were abolished by miR‐506‐3p downregulation or KAT6B sufficiency. Our study suggests that circ‐MALAT1 could sponge miR‐506‐3p to regulate the expression of KAT6B. Moreover, KAT6B sufficiency could neutralize miR‐506‐3p‐dependent growth arrest, migration, and EMT. Circ‐MALAT1 promotes cell proliferation, migration, and EMT of CRC cells via the miR‐506‐3p/KAT6B axis, thereby acting as a novel potential therapeutic target for the treatment of colorectal cancer.https://doi.org/10.1002/kjm2.12698circ‐MALAT1colorectal cancerEMTKAT6BmiR‐506‐3p
spellingShingle Feng‐Shuai Yang
Shuang‐Xi Gong
Dong‐Da Qiu
Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis
Kaohsiung Journal of Medical Sciences
circ‐MALAT1
colorectal cancer
EMT
KAT6B
miR‐506‐3p
title Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis
title_full Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis
title_fullStr Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis
title_full_unstemmed Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis
title_short Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis
title_sort circ malat1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating mir 506 3p kat6b axis
topic circ‐MALAT1
colorectal cancer
EMT
KAT6B
miR‐506‐3p
url https://doi.org/10.1002/kjm2.12698
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AT shuangxigong circmalat1acceleratescellproliferationandepithelialmesenchymaltransformationofcolorectalcancerthroughregulatingmir5063pkat6baxis
AT dongdaqiu circmalat1acceleratescellproliferationandepithelialmesenchymaltransformationofcolorectalcancerthroughregulatingmir5063pkat6baxis