MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells

Abstract The transcription factor MYB proto-oncogene like 2 (MYBL2) has been reported to be involved in the occurrence and development of various tumors, however, its role in gastric cancer (GC) remains to be elucidated. In this study, the Kaplan-Meier plotter was used to evaluate the prognostic val...

Full description

Saved in:
Bibliographic Details
Main Authors: Jingya Chen, Zhenglei Ji, Di Wu, Siyang Wei, Wanjing Zhu, Guisen Peng, Mingjie Hu, Yunli Zhao, Huazhang Wu
Format: Article
Language:English
Published: Nature Portfolio 2025-03-01
Series:Scientific Reports
Subjects:
Online Access:https://doi.org/10.1038/s41598-025-93022-4
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849389895022280704
author Jingya Chen
Zhenglei Ji
Di Wu
Siyang Wei
Wanjing Zhu
Guisen Peng
Mingjie Hu
Yunli Zhao
Huazhang Wu
author_facet Jingya Chen
Zhenglei Ji
Di Wu
Siyang Wei
Wanjing Zhu
Guisen Peng
Mingjie Hu
Yunli Zhao
Huazhang Wu
author_sort Jingya Chen
collection DOAJ
description Abstract The transcription factor MYB proto-oncogene like 2 (MYBL2) has been reported to be involved in the occurrence and development of various tumors, however, its role in gastric cancer (GC) remains to be elucidated. In this study, the Kaplan-Meier plotter was used to evaluate the prognostic value of different MYBL2 expression levels in GC patients. The UALCAN database were applied to analyze the relationships between MYBL2 and clinicopathological characteristics of GC. GC cell proliferation, cell cycle and apoptosis were determined by CCK-8 and flow cytometry assays, and proteins were examined by Western blot analysis. Next, signaling pathway enrichment analysis of MYBL2-related genes and protein expression were analyzed by Gene Set Enrichment Analysis (GSEA) and Western blot assays. The results found that MYBL2 expression was significantly upregulated in GC compared with adjacent non-malignant tissues and associated with poor patient survival, tumor, stages and lymph node metastasis. Forced expression of MYBL2 could promote cell proliferation, resulting in an accelerated S phase progression and inhibiting cell apoptosis in GC cells. Conversely, MYBL2 silencing inhibited cell proliferation, induced G2/M phase arrest and promoted cell apoptosis in GC cells. Mechanistically, Western blot analysis showed that MYBL2 silencing decreased the expression of BCL2 and upregulated the expression of Cleaved-caspase-3 and BAX in HGC-27 cells. Conversely, MYBL2 overexpression in AGS cells resulted in the opposite effects. Furthermore, enforced expression of MYBL2 activated the PI3K/AKT signaling pathway, especially AKT phosphorylation. Additionally, the AKT inhibitor MK2206 significantly reversed the proliferation capacity of GC cells induced by MYBL2 overexpression. Therefore, these results suggest that upregulated expression of MYBL2 contributes to GC cell growth and inhibits cell apoptosis by regulating the PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathways in GC cells indicating that MYBL2 may be a new therapeutic target and prognostic marker for GC.
format Article
id doaj-art-2b2cfc0ecfcf475f944fdc5f74161da1
institution Kabale University
issn 2045-2322
language English
publishDate 2025-03-01
publisher Nature Portfolio
record_format Article
series Scientific Reports
spelling doaj-art-2b2cfc0ecfcf475f944fdc5f74161da12025-08-20T03:41:49ZengNature PortfolioScientific Reports2045-23222025-03-0115111110.1038/s41598-025-93022-4MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cellsJingya Chen0Zhenglei Ji1Di Wu2Siyang Wei3Wanjing Zhu4Guisen Peng5Mingjie Hu6Yunli Zhao7Huazhang Wu8School of Public Health, Bengbu Medical UniversitySchool of Public Health, Bengbu Medical UniversitySchool of Life Science, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical UniversitySchool of Public Health, Bengbu Medical UniversitySchool of Life Science, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical UniversitySchool of Life Science, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical UniversitySchool of Life Science, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical UniversitySchool of Public Health, Bengbu Medical UniversitySchool of Life Science, Anhui Provincial Key Laboratory of Tumor Evolution and Intelligent Diagnosis and Treatment, Bengbu Medical UniversityAbstract The transcription factor MYB proto-oncogene like 2 (MYBL2) has been reported to be involved in the occurrence and development of various tumors, however, its role in gastric cancer (GC) remains to be elucidated. In this study, the Kaplan-Meier plotter was used to evaluate the prognostic value of different MYBL2 expression levels in GC patients. The UALCAN database were applied to analyze the relationships between MYBL2 and clinicopathological characteristics of GC. GC cell proliferation, cell cycle and apoptosis were determined by CCK-8 and flow cytometry assays, and proteins were examined by Western blot analysis. Next, signaling pathway enrichment analysis of MYBL2-related genes and protein expression were analyzed by Gene Set Enrichment Analysis (GSEA) and Western blot assays. The results found that MYBL2 expression was significantly upregulated in GC compared with adjacent non-malignant tissues and associated with poor patient survival, tumor, stages and lymph node metastasis. Forced expression of MYBL2 could promote cell proliferation, resulting in an accelerated S phase progression and inhibiting cell apoptosis in GC cells. Conversely, MYBL2 silencing inhibited cell proliferation, induced G2/M phase arrest and promoted cell apoptosis in GC cells. Mechanistically, Western blot analysis showed that MYBL2 silencing decreased the expression of BCL2 and upregulated the expression of Cleaved-caspase-3 and BAX in HGC-27 cells. Conversely, MYBL2 overexpression in AGS cells resulted in the opposite effects. Furthermore, enforced expression of MYBL2 activated the PI3K/AKT signaling pathway, especially AKT phosphorylation. Additionally, the AKT inhibitor MK2206 significantly reversed the proliferation capacity of GC cells induced by MYBL2 overexpression. Therefore, these results suggest that upregulated expression of MYBL2 contributes to GC cell growth and inhibits cell apoptosis by regulating the PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathways in GC cells indicating that MYBL2 may be a new therapeutic target and prognostic marker for GC.https://doi.org/10.1038/s41598-025-93022-4MYBL2Cell proliferationCell apoptosisPI3K/AKT signaling pathwayGastric cancer
spellingShingle Jingya Chen
Zhenglei Ji
Di Wu
Siyang Wei
Wanjing Zhu
Guisen Peng
Mingjie Hu
Yunli Zhao
Huazhang Wu
MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells
Scientific Reports
MYBL2
Cell proliferation
Cell apoptosis
PI3K/AKT signaling pathway
Gastric cancer
title MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells
title_full MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells
title_fullStr MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells
title_full_unstemmed MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells
title_short MYBL2 promotes cell proliferation and inhibits cell apoptosis via PI3K/AKT and BCL2/BAX/Cleaved-caspase-3 signaling pathway in gastric cancer cells
title_sort mybl2 promotes cell proliferation and inhibits cell apoptosis via pi3k akt and bcl2 bax cleaved caspase 3 signaling pathway in gastric cancer cells
topic MYBL2
Cell proliferation
Cell apoptosis
PI3K/AKT signaling pathway
Gastric cancer
url https://doi.org/10.1038/s41598-025-93022-4
work_keys_str_mv AT jingyachen mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT zhengleiji mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT diwu mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT siyangwei mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT wanjingzhu mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT guisenpeng mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT mingjiehu mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT yunlizhao mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells
AT huazhangwu mybl2promotescellproliferationandinhibitscellapoptosisviapi3kaktandbcl2baxcleavedcaspase3signalingpathwayingastriccancercells