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The p38/mapk pathway as a therapeutic target to prevent therapeutic escape of breast cancer stem cells

Science China(Life Sciences) 2024年第9期67卷 1867-1880页

作者： Weixiao Yan Xiaotong Wang Wenjing Wang Qi Guo Na Huang Hao Chen Xing-Jie Liang Yu Han Dandan Liu Jinchao Zhang State Key Laboratory of New pharmaceutical preparations and Excipients/Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education/College of Chemistry and Materials Science Chemical Biology Key Laboratory of Hebei ProvinceHebei UniversityBaoding 071002China CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety National Center for Nanoscience and TechnologyBeijing 100190China

Cancer stem cells(CSCs)play an important role in metastasis development,tumor recurrence,and treatment resistance,and are essential for the eradication of ***,therapies fail to eradicate CSCs due to their therapeutic stress-induced cellular escape,which leads to enhanced aggressive behaviors compared with CSCs that have never been ***,the underlying mechanisms regulating the therapeutic escape remain *** this end,we established a model to isolate the therapeutic escaped CSCs(TSCSCs)from breast CSCs and performed the transcription profile to reveal the ***,we demonstrated that the behavior of therapeutic escape was regulated through the p38/mapk signaling pathway,resulting in TSCSCs exhibiting enhanced motility and ***,blocking the p38/mapk signaling pathway effectively reduced motility and metastasis ability both in vitro and in vivo,which were further supported by downregulated motility-related genes and epithelial-mesenchymal transition(EMT)-related proteins vimentin and *** obtained findings reveal the p38/mapk pathway as a potential therapeutic target for TSCSCs and would provide profound implications for cancer therapy.

关键词： therapeutic escape breast cancer stem cells motility p38/mapk signaling pathway molecular mechanism

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The functional analysis of transiently upregulated miR-101 suggests a “braking” regulatory mechanism during myogenesis

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Science China(Life Sciences) 2021年第10期64卷 1612-1623页

作者： Shurong Liu Shujuan Xie Huafeng Chen Bin Li Zhirong Chen Yeya Tan Jianhua Yang Lingling Zheng Zhendong Xiao Qi Zhang Lianghu Qu MOE Key Laboratory of Gene Function and Regulation State Key Laboratory of BiocontrolSchool of Life SciencesSun Yat-sen UniversityGuangzhou 510275China Vaccine Research Institute of Sun Yat-sen University the Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510630China Cell-Gene Therapy Translational Medicine Research Center the Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhou 510630China

Skeletal muscle differentiation is a highly coordinated process that involves many cellular signaling pathways and microRNAs(miRNAs).A group of muscle-specific miRNAs has been reported to promote myogenesis by suppressing key signaling pathways for cell ***,the functional role and regulatory mechanism of most non-muscle-specific miRNAs with stage-specific changes during differentiation are largely ***,we describe the functional characterization of miR-101a/b,a pair of non-muscle-specific miRNAs that show the largest change among a group of transiently upregulated miRNAs during myogenesis in C2C12 *** overexpression of miR-101a/b inhibits myoblast differentiation by suppressing the p38/mapk,Interferon Gamma,and Wnt pathways and enhancing the C/EBp ***2a,a key protein in the p38/mapk pathway,was identified as a direct target of miR-101a/***,we found that the long non-coding RNA(lncRNA)Malat1,which promotes muscle differentiation,interacts with miR-101a/b,and this interaction competes with Mef2a mRNA to relieve the inhibition of the p38/mapk pathway during *** results uncovered a“braking”role in differentiation of transiently upregulated miRNAs and provided new insights into the competing endogenous RNA(ceRNA)regulatory mechanism in myoblast differentiation and myogenesis.

关键词： miR-101a/b p38/mapk signaling pathway Mef2a Malat1 skeletal muscle differentiation

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